< Presentation of case >
The 36-year-old woman, previously healthy, was admitted because of persistent headache and fever. Four days prior to this admission, she began to develop fever up to 39℃, myalgias, rhinorrhea and cough. Her colleagues had reported similar symptoms. She sought medical attention at a local clinic and influenza rapid test revealed positive for influenza A. Oseltamivir 75 mg bid was prescribed. On the second day, fever subsided but headache with nausea occurred. She came to our emergency department and acute gastroenteritis was impressed. Due to persistent headache and nausea, she came to our emergency department again on the fourth day.
She denied recent travel, a history of cluster or contact with animals. She did not smoke or consume alcohol.
On examination, she was conscious and orientated to time, person, and place. The temperature was 37.3℃, the pulse rate 104 beats per minute, blood pressure 114/80 mmHg, and the respiratory rate 19 breaths per minutes. Neck was stiff. On neurological examination, no focal neurological deficieny was noted. Other physical examinations were unremarkable.
At the emergency department, computed tomography of the brain revealed no space-occupying lesion but mild swelling of the cerebrum. A white blood-cell count of a blood specimen was 13,000 per μL and urine analysis revealed a white blood-cell count of 35-50 per high power field (HPF). A lumbar puncture was performed and analysis of the cerebrospinal fluid (CSF) specimen revealed a white blood-cell count of 1,890 (*11/9 perμL) with lymphocyte/neutrophil 21/79, glucose 30 mg/dL (serum glucose was 98 mg/dL), total protein 111.4 mg/dL, and red blood-cell count 90 perμL; opening pressure was 238 mmH2O. India ink smear of the CSF specimen was reported negative. Ceftriaxone was administrated intravenously. She was admitted to our isolated room for further treatment.
After admission, bacterial culture of a CSF specimen yielded Neisseria meningitidis and blood culture yielded no pathogen. Right knee pain with swelling and local heat was noted. Arthrocentesis was performed for obtain synovial fluid for analysis and cultures; pus cells >30 cells per oil immersion field was found while cultures revealed no growth. Lumbar puncture was repeated on the 8th day of ceftriaxone treatment, which reported a white blood-cell count of 2 (*11/9 perμL). Headache and knee pain and swelling resolved. She was discharged.
< Discussion >
In this case, we described a case of meningococcal meningitis who presented with new-onset persistent headache with nausea after influenza A infection.
Epidemic cerebrospinal fever (meningococcal meningitis) was first described in Geneva by Vieusseaux in 1805. Subsequent reports throughout the 19th century confirmed its episodic, epidemic nature with a propensity for afflicting young children and military recruits assembled in stationary barracks situations. In 1887, Weichselbaum isolated the meningococcus from cerebrospinal fluid, and the etiologic relationship between this organism and epidemic meningitis was firmly established. Kiefer in 1896 and Albrecht and Ghon in 1901 found that healthy persons could become carriers of the meningococcus. Serotypes of the meningococcus were first recognized by Dopter in 1909.
Neisseria meningitidis is a gram-negative diplococcus. The organism produces a polysaccharide capsule, which is the basis of the serogroup typing system. Optimal growth conditions are achieved in a moist environment at 35 to 37℃ under an atmosphere of 5% to 10% carbon dioxide. Confirmation of the presence of this organism in clinical specimens is dependent on a series of carbohydrate fermentations or polymerase chain reaction techniques. Meningococci can now be segregated by seroagglutination into at least 13 serogroups: A, B, C, D, X, Y, Z; E, W-135, H, I, K, and L.
Meningococcal disease occurs worldwide as isolated cases, institution- or community-based outbreaks, and large epidemics. Meningococci that colonize the upper respiratory tract are internalized by non-ciliated mucosal cells and may them to enter the submucosa, from which they can make their way into the bloodstream. A meningococcal organism that enters the bloodstream from the nasopharynx and survives host defenses generally has one of two fates. If multiplication occurs slowly, the bacteria eventually may seed local sites, such as the meninges and/or (rarely) the joints or the pericardium. More rapid multiplication in the bloodstream is associated with the clinical features of meningococcemia.
Epidemiologic data on N. meningitides infection are scarcely published in Taiwan. A nationwide study was conducted to retrospectively analyze epidemiologic data from 115 patients with laboratory confirmed meningococcal disease that occurred in Taiwan from 2001 through 2003. Serogroup W135 accounted for 26% of all cases and most (76.7%) were older than 20 years. There were no cases of serogroup W135 meningococcal disease associated with Hajj pilgrims, and all cases were sporadic.
Common presenting symptoms of patients with meningococcal meningitis include nausea and vomiting, headache, neck stiffness, lethargy and confusion. The symptoms and signs of meningococcal meningitis cannot be distinguished form those elicited by other meningeal pathogens. CSF findings are consistent with those of purulent meningitis: hypoglycorrhachia, an elevated protein concentration, and a neutrophilic leukocytosis. The definitive diagnosis is established by recovering Neisseria meningitidis, its antigens, or its DNA from normal sterile body fluid.
In the epidemiologic study in Taiwan mentioned earlier, the presenting symptoms, signs, laboratory data, and outcomes of 88 patients with complete case records were compared between patients infected with W135 and with non-W135. No differences in presenting symptoms were found except for the higher prevalence of pneumonia found in W135 patients (23.8% vs. 1.5%; OR: 20.6; 95%CI: 2.3-189.0; P=0.003). The distribution of inflammatory cells in CSF in patients with meningitis was also different between patients infected with W135 and with non-W135. Patients infected with W135 were more likely to develop respiratory failure requiring intubations and shock, though it did not achieve statistical significance. In multivariate analysis, three independent factors associated with death were found: bacteremia without meningitis, altered mental status, and petechiae or purpura on admission.
A third-generation cephalosporin is preferred for initial therapy. Penicillin G remains an acceptable alternative for confirmed invasive meningococcal disease in most countries. Other options include meropenem. The newer fluoroquinolones have excellent in vitro activity against N. meningitides, with measurable central nervous system penetration, and appear promising in animal models. Glucocorticoid therapy for meningococcal meningitis in adult is controversial. In addition to the use of antibiotics, the application of supportive care to treat the problems of DIC, shock, heart failure, prolonged mental obtundation, pericarditis, and pneumonia, which complicate this infection, had had a decided impact on prognosis. A tetravalent serogroup A, C, Y, and W-135 capsular polysaccharide vaccine has been approved for use. A tetravalent vaccine conjugate vaccine (A, C, Y, and W-135) has been approved for use in the United States in 2005. Close contacts of cases should receive chemoprophylaxis with rifampin, ciprofloxacin, ofloxacin, azithromycin or ceftriaxone.
< References >
- Principles and Practice of Infectious Diseases. 7th edition.
- Harrison’s Principles of Internal Medicine 17th edition.
- Wang JL, et al. BMC Infect Dis 2006;6:7.
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Case Discussion
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