Meningococcal infections

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: The influence of genomics and proteomics on the development of potential vaccines against meningococcal infection

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Other Syndromes Local extension causing empyema is very uncommon, and—as might be inferred from the low rate of bacteremia—metastatic complications of M. catarrhalis pneumonia, such as septic arthritis, are exceedingly rare. As of 1995, 58 cases of bacteremic infection due to M. catarrhalis had been reported, mainly in children 60 years old; most of these patients had severe underlying lung disease and/or were immunocompromised. The syndromes reported have included bacteremia with no apparent focus, pneumonia, endocarditis, and meningitis.

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Antimicrobial Chemoprophylaxis The attack rate for meningococcal disease among household or other close contacts of cases is 400-fold greater than that in the population as a whole. Close contacts of cases should receive chemoprophylaxis with rifampin, ciprofloxacin, ofloxacin, or azithromycin (Table 136-1). A single IM injection of ceftriaxone is also effective. Close contacts include persons who live in the same household, day-care center contacts, and anyone directly exposed to a patient's oral secretions. Casual contacts are not at increased risk.

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Association of Virulence Mechanisms with Specific Meningococcal Infections Specific disease manifestations of meningococcal infections have specific virulence and pathogenic mechanisms, as described below for fulminant meningococcemia and meningitis. Fulminant Meningococcemia Purpura Fulminans Fulminant meningococcemia is perhaps the most rapidly lethal form of septic shock experienced by humans. It differs from most other forms of septic shock by the prominence of hemorrhagic skin lesions (petechiae, purpura; see Fig. 52-5) and the consistent development of DIC.

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Host Defense Mechanisms Preventing meningococcal growth in blood requires bactericidal and opsonic antibodies, complement, and phagocytes (Fig. 136-3). The major bactericidal antibodies are IgM and IgG, which (except for serogroup B) bind to the capsular polysaccharide. Immunity to meningococci is therefore serogroup specific. Antibodies to other surface (subcapsular) antigens may confer crossserogroup protection. PorA, PorB, Opc, and LOS appear to be major targets of cross-reactivity and of serogroup B bactericidal antibodies.

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Patients with fulminant meningococcemia often experience diffuse leakage of fluid into extravascular spaces, shock, and multiple-organ dysfunction (Chaps. 264 and 265). Myocardial depression may be prominent. Supportive therapy, although never studied in randomized, placebo-controlled trials, is recommended. Standard measures include vigorous fluid resuscitation (often requiring several liters over the first 24 h), elective ventilation, and pressors. Some authorities recommend early hemodialysis or hemofiltration.

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Clinical Manifestations Upper Respiratory Tract Infections Although many patients who develop meningococcal meningitis or meningococcemia report having had throat soreness or other upper respiratory symptoms during the preceding week, it is uncertain whether these symptoms are due to infection with meningococci. Meningococcal pharyngitis is rarely diagnosed. Adult patients with N. meningitidis bacteremia more often have clinically apparent disease of the respiratory tract (pneumonia, sinusitis, tracheobronchitis, conjunctivitis) than do younger patients.

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Complications Patients with meningococcal meningitis may develop cranial nerve palsies, cortical venous thrombophlebitis, and cerebral edema. Children may develop subdural effusions. Permanent sequelae can include mental retardation, deafness, and hemiparesis. The major long-term morbidity of fulminant meningococcemia is the loss of skin, limbs, or digits that results from ischemic necrosis and infarction. Diagnosis Few clinical clues help the physician distinguish the patient with early meningococcal disease from patients with other acute systemic infections. ...

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In the United States, the attack rate for sporadic meningococcal disease is ~1 case per 100,000 persons per year. Disease attack rates are highest among infants 3–9 months of age (10–15 cases per 100,000 infants per year). Attack rates are higher among children than among adults, and there is a second peak of incidence among teenagers, in whom outbreaks have often been tied to residence in barracks, dormitories, or other crowded conditions.

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Outer-Membrane Components Associated with Virulence Meningococcal strains are characterized by the expression of capsular polysaccharide and other outer-membrane structures, including LOS (endotoxin). Outer-membrane blebbing, meningococcal autolysis, molecular mimicry, genome plasticity, horizontal DNA exchange, and phase and/or antigenic variation are all important in meningococcal virulence. Capsule The polysaccharide capsule is a major—if not the major—virulence factor of N. meningitidis.

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Harrison's Internal Medicine Chapter 136. Meningococcal Infections Definition Neisseria meningitidis is the etiologic agent of two life-threatening diseases: meningococcal meningitis and fulminant meningococcemia. More rarely, meningococci cause pneumonia, septic arthritis, pericarditis, urethritis, and conjunctivitis. Most cases are potentially preventable by vaccination. Etiologic Agent Meningococci are gram-negative aerobic diplococci. Unlike the other neisseriae, they have a polysaccharide capsule.

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Sepsis with Skin Manifestations (See also Chap. 18) Maculopapular rashes may reflect early meningococcal or rickettsial disease but are usually associated with nonemergent infections. Exanthems are usually viral. Primary HIV infection commonly presents with a rash that is typically maculopapular and involves the upper part of the body but can spread to the palms and soles. The patient is usually febrile and can have lymphadenopathy, severe headache, dysphagia, diarrhea, myalgias, and arthralgias.

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Purpura Fulminans (See also Chaps. 136 and 265) Purpura fulminans is the cutaneous manifestation of DIC and presents as large ecchymotic areas and hemorrhagic bullae. Progression of petechiae to purpura, ecchymoses, and gangrene is associated with congestive heart failure, septic shock, acute renal failure, acidosis, hypoxia, hypotension, and death. Purpura fulminans has been associated primarily with N. meningitidis but, in splenectomized patients, may be associated with S. pneumoniae and H. influenzae.

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