Fiore A E, Iverson C, Messmer T, Erdman D, Lett S M, Talkington D F, Anderson L J, Fields B, Carlone G M, Breiman R F, Cetron M S
Epidemic Intelligence Service, Epidemiology Program Office, Centers for Disease Control and Prevention, Public Health Service, United States Department of Health and Human Services, Atlanta, Georgia 30333, USA.
J Am Geriatr Soc. 1998 Sep;46(9):1112-7. doi: 10.1111/j.1532-5415.1998.tb06649.x.
To determine the causes of an outbreak of lobar pneumonia.
Matched (1:2) case-control study.
A 70-bed chronic care facility for older people.
Residents of the facility.
Ten residents developed pneumonia over a 10-day period. Two residents died. One case-patient had Streptococcus pneumoniae bacteremia; another had polymerase chain reaction evidence of S. pneumoniae infection. No other etiologic agent was identified. Only four of 10 case-patients had received routine diagnostic cultures of blood or sputum before the administration of antibiotics. Symptoms of upper respiratory illness (URI) among residents before the pneumonia outbreak corresponded with elevation of antibodies to human parainfluenza virus 1 (HPIV1). In a matched case-control study, six of 10 case-patients, compared with five of 20 controls, had symptoms of URI during the preceding month (matched odds ratio (MOR) = 4.5, 95% CI = 0.8-33). Nine case-patients had serum available, and five of these had both serologic evidence of recent HPIV1 infection and recent URI, compared with two of 18 controls (MOR = 9.0, 95% CI = 1.2-208). Only three residents had documentation of pneumococcal vaccination.
Noninfluenza viral infections may play a role in the pathogenesis of some bacterial pneumonias. S. pneumoniae was the cause of at least two pneumonias; lack of preantibiotic cultures may have interfered with isolation of S. pneumoniae in others. Recent HPIV1 infection was epidemiologically linked to subsequently developing pneumonia. Spread of HPIV1 in the facility may have contributed to increased susceptibility to S. pneumoniae and, potentially, to other bacterial pathogens.
确定大叶性肺炎暴发的原因。
配对(1:2)病例对照研究。
一家拥有70张床位的老年人慢性病护理机构。
该机构的居民。
10名居民在10天内患上肺炎。2名居民死亡。1例患者有肺炎链球菌菌血症;另一例有肺炎链球菌感染的聚合酶链反应证据。未发现其他病原体。10例患者中只有4例在使用抗生素前接受了血液或痰液的常规诊断培养。肺炎暴发前居民的上呼吸道疾病(URI)症状与人类副流感病毒1型(HPIV1)抗体升高相对应。在一项配对病例对照研究中,10例患者中有6例在之前一个月出现URI症状,而20例对照中有5例出现(配对比值比(MOR)=4.5,95%置信区间=0.8-33)。9例患者有血清样本,其中5例既有近期HPIV1感染的血清学证据又有近期URI,而18例对照中有2例(MOR=9.0,95%置信区间=1.2-208)。只有3名居民有肺炎球菌疫苗接种记录。
非流感病毒感染可能在某些细菌性肺炎的发病机制中起作用。肺炎链球菌是至少两例肺炎的病因;抗生素使用前未进行培养可能妨碍了其他病例中肺炎链球菌的分离。近期HPIV1感染在流行病学上与随后发生的肺炎有关。HPIV1在该机构中的传播可能导致对肺炎链球菌及其他潜在细菌病原体的易感性增加。