We present case of a 34-year-old man who presented to the emergency department with one-day history of acute generalised abdominal pain, nausea, vomiting and fever with rigors.

He also complained of mild 4/10 generalised headache without photophobia. He denied any urinary, bowel or respiratory symptoms. He had no previous significant medical history of note. He is a non-smoker and a teetotaller, and works in a retail shop. 

On arrival to the ED he was tachycardic and hypotensive with generalised guarding and tenderness all over the abdomen. On systemic examination he was pale, dehydrated without any neck stiffness, focal neurology and Kernig and Brudzinski signs were negative. Cardiovascular system, central nervous system and chest examinations were unremarkable. There was no rash, petechiae or ecchymosis.

Sepsis protocol was initiated and routine bloods revealed markedly raised inflammatory markers with deranged renal functions (acute kidney injury) and cholestatic picture of liver function tests (LFTs) with raised bilirubin, alkaline phosphatase (ALP) and gamma glutamyltransferase (GGT). 

The working diagnosis was abdominal sepsis/leptospirosis/cholangitis. The surgical team was consulted and CT abdomen was performed which was unremarkable with no acute surgical cause of his symptoms. He was not responsive to fluid resuscitation and was commenced on empirical broad spectrum antibiotics and inotropes with ICU admission and central venous pressure (CVP) monitoring. His chest x-ray, echocardiogram and urine microscopy did not show any abnormality. Bloods cultures turned out to be the most significant investigation as there was growth of gram-negative diplococci isolated on culture which was later confirmed to be Neisseria meningitidis. His cerebrospinal fluid (CSF) culture and PCR was negative without any growth. Throat swab and urethral swab did not reveal any organisms. He was switched to ceftriaxone 2gm bid IV as per sensitivities and had a complete course of seven days in accordance with microbiology consultation.

He made a good recovery within 48 hours of commencing ceftriaxone and clinical parameters normalised, without the need for inotropic support. His renal function returned to baseline and liver function showed a downward trend and improvement.

Nisseria meningitidis serogroup Y was later confirmed as the causative agent. 

The patient was screened for HIV and hepatitis which were negative with normal immunoglobulins and complement levels. He was discharged after seven days of intravenous antibiotic treatment and the case was notified to the Health Protection Surveillance Centre.

Discussion

Neisseria meningitides is a gram negative diplococcic which infects humans with a mortality of approximately 13%, despite antibiotic treatment.¹ The clinical manifestations of meningococcal disease can be quite varied.²

The organism is divided into 12 antigenically distinct serogroups (A, B, C, E, H, I, K, L, W, X, Y and Z). In Ireland, serogroup B and C strains account for over 99% of all meningococcal disease. Patients with C3 deficiency are at high risk of severe infection with meningococcal strain. Meningococcal disease in those with C5-C8 deficiencies is almost always caused by serogroup W, Y or E, and is typically recurrent.⁷ Acute systemic meningococcal disease most frequently manifests itself by three syndromes: meningitis alone, meningitis with accompanying meningococcaemia and meningococcaemia without clinical evidence of meningitis.³

In a prospective observational cohort study, the classic meningitis triad of fever, neck stiffness and altered mental status was present in 70 of the 258 patients (27%) with meningococcal meningitis; when rash was added, 89% of patients had at least two of these four signs.² Myalgias and preceding symptoms of pharyngitis can be present. Over 50% of patients will have petechiae on presentation. Focal neurologic signs and seizures are less common in meningococcal meningitis. Myocardial and abdominal involvement is rare.⁸ In a case series of invasive meningococcal disease in France, 105 patients presented with abdominal pain and gastroenteritis.⁸ Disease progression is usually rapid with transition from health to severe disease in a matter of hours.⁴

The difficulty in identifying meningococcal disease is due, in part, to the fact that clinicians in the community see so few cases in their lifetime and that the classic clinical features of meningococcal disease (eg. haemorrhagic rash, meningism and impaired consciousness) appear late in the illness.

The patient presents with low blood pressure with an elevated pulse rate. An intensive search for petechiae and ecchymoses should be undertaken. The physical examination should also include provocative tests for meningeal irritability, such as the Kernig and Brudzinski signs. Meningococcal meningitis and meningococcaemia often result in shock, disseminated intravascular coagulation and purpura fulminans.⁶

The gold standard for the diagnosis of systemic meningococcal infection is the isolation of Neisseria meningitides by culture from a usually sterile body fluid, such as blood (positive in 50-60%) or cerebrospinal fluid (CSF positive in 80-90%), or, less commonly, synovial, pleural, or pericardial fluid. The gram stain and culture of skin biopsies increase the yield.⁹

Early and appropriate antibiotic treatment markedly improves the outcome.¹⁰

References

1. Kim GY, Sorvillo F, Kuo T. Update on meningococcal disease mortality in the United States since 2002. Pediatr Infect Dis J 2010; 29:681
2. Heckenberg SG, de Gans J, Brouwer MC et al. Clinical features, outcome, and meningococcal genotype in 258 adults with meningococcal meningitis: a prospective cohort study. Medicine (Baltimore) 2008; 87:185
3. Durand ML, Calderwood SB, Weber DJ et al. Acute bacterial meningitis in adults. A review of 493 episodes. N Engl J Med 1993; 328:21
4. van de Beek D, de Gans J, Spanjaard L et al. Clinical features and prognostic factors in adults with bacterial meningitis. N Engl J Med 2004; 351:1849
5. Carpenter RR, Petersdorf RG. The clinical spectrum of bacterial meningitis. Am J Med 1962; 33:262
6. Darmstadt GL. Acute infectious purpura fulminans: pathogenesis and medical management. Pediatr Dermatol 1998; 15:169
7. Brandtzaeg P, Mollnes TE, Kierulf P. Complement activation and endotoxin levels in systemic meningococcal disease. J Infect Dis 1989; 160:58
8. Koppes GM, Ellenbogen C, Gebhart RJ. Group Y meningococcal disease in United States Air Force recruits. Am J Med 1977; 62:661
9. Hoyne AL, Brown RH. Seven hundred and twenty seven meningococcic cases; an analysis. Ann Intern Med 1948; 28:248
10. Levin S, Painter MB. The treatment of acute meningococcal infection in adults. A reappraisal. Ann Intern Med 1966; 64:1049