Age: 19.0
Sex: M
Vaccine: MNQ
Symptoms: White blood cell count normal, pH body fluid decreased
Clinical narrative: Case number PHHY2013US033977 is an initial literature report on 09 Jan 2013. In this article, the author discussed about a case with meningococcal polysaccharide vaccine failure in a patient with C7 (complement) deficiency and a decreased anti-capsular antibody response. This report refers to a 20-year-old male patient. At the age of 10 years he had fever, headache, body aches, photophobia, neck stiffness, petechiae, lumbar puncture showed pleocytosis and gram-negative diplococcic, rash and platelet count decreased (94 x 10^3/mm3). His cerebrospinal fluid (CSF) cultures showed presence of Neisseria meningitides (diagnosis of meningococcal meningitis) and received treatment with dexamethasone, ampicillin, and meropenem and his CH50 (classical complement pathway hemolytic assay) was 40 u/Ml. While he was in good health, before vaccination, his complement levels was as followed, C6: 10.4 mg/dL, C7: undetected; C8: 19.8 mg/dL and C9: 31 mg/dL. At the age of 19, he was vaccinated with tetravalent polysaccharide meningococcal vaccine (manufacturer and batch number: unknown, conservatively taken as MENVEO INN) on an unspecified date. After 10 months of post vaccination (five months before his terminal illness), his serum sample showed IgG levels to capsular polysaccharides as group A capsule: 3.5 mg/mL; group C capsule: less than 0.5 mg/mL; group Y capsule: 0.8 mg/mL and group W-135 capsule: less than 0.5 mg/mL. It was reported complement component 7 was found to be deficient and antibody levels to meningococcal polysaccharides were undetectable for two serogroups and low for the infecting serogroup 10 months post-vaccination. After 15 months of vaccination, he presented to a clinic for one day history of fever, chills, aching in the muscles of his legs, upper back and neck and a pounding frontal headache with light sensitivity. At this initial clinic visit he was diagnosed with a probable viral syndrome, and was prescribed with ibuprofen, and excused from duty for the day. About 8 hours later he developed nausea, vomiting and a generalized purplish macular rash. He said he felt like he did when he had meningitis. He visited the emergency room (hospitalization), and had respiratory distress, on his arrival, prompting endotracheal intubation. His lab tests showed white blood cell count : 5.2 x 10^3/mm3, platelet count: 23 x 10^3/mm3, creatinine: 2.42 mg/dL, prothrombin time: 31.6 sec, activated partial thromboplastin time: 131.9 sec and arterial pH: 7.20. He presented with symptoms of meningococcal sepsis and started treatment with several broad-spectrum antibiotics, including ceftriaxone, and dexamethasone. His CH50, drawn while he was in the throes of sepsis was 10 U/mL; C3 was low at 62 mg/dL and C4 was low at 10 mg/dL. His blood cultures showed presence of N. meningitides, which was subsequently showed to be serogroup Y. Despite pressor support, transfusions of fresh frozen plasma and hemodialysis, he expired due to disseminated intravascular coagulation and intracranial hemorrhage on hospital day of 6. The author stated that the anti-capsular IgG (immunoglobulin G) levels of the patient appeared to be modest for group A, but clearly deficient to group C and his antibodies to group W-135 were undetectable and to group Y were clinically inadequate, hence represent the earliest time to vaccine failure in a C7-deficient individual in which the infecting serogroup and prior antibody levels were known. This case highlight the fact that some individuals with terminal complement component deficiencies (TCCD) mount an impaired or short-lived response to vaccination with meningococcal capsular polysaccharides and underscore the appropriateness of a more aggressive vaccination strategy in this patient population.