C. pneumoniae: community acquired pneumonia and respiratory infections.

Numerous serological studies have confirmed that C. pneumoniae is a cause of community acquired pneumonia throughout the world. In most instances, the diagnosis has been based on a significant increase in specific IgG titres. In a prospective study from a general population in Seattle, where serum specimens were collected twice a year and also at times of illness, specific IgG titre rises were not seen in children under the age of 5. The incidence was at its highest with an annual rate of 9.2% in those aged between 5 to 10 and it dropped to 1.5% in those over 20 [Aldous et al., 1992]. It was not reported how many of the seroconversion episodes were associated with illness except that in children one third of episodes were asymptomatic [Aldous et al., 1990]. In fact, it is unlikely that all seroconversion episodes were associated with community acquired pneumonia. For instance, the incidence of community acquired pneumonia in the United Kingdom is approximately 0.1% per year. In studies which have looked specifically at adults with community acquired pneumonia, C. pneumoniae was the causative agent in 3.4% to 43% of cases [Gaydos, et al., 1994; Fang et al., 1990; Lieberman et al., 1996; Kaupinnen et al., 1995]. It was never the most common aetiological agent and co-infection with a second organism was often present [Fang et al., 1990; Kauppinen et al., 1995]. If it is assumed in adults, that the annual incidence of community acquired pneumonia is 0.1%, that C. pneumoniae is responsible for 10% of these and that the annual seroconversion rate is 1.5%, then only 1 in 150 C. pneumoniae infections will result in pneumonia. Apart from pneumonia, there is limited evidence that C. pneumoniae can also cause upper respiratory tract infections [Hammerschlag, 2000] but it has been suggested that 90% or more of C. pneumoniae infections are asymptomatic [Kleemola et al., 1988]. It is possible that the incidence of asymptomatic acute infection is even higher than the Seattle data suggests. This is because seroconversion may not always be present. In one study, only 3 of 8 culture positive patients had serologic evidence of acute infection [Chirgwin et al., 1991].

Apart from acute respiratory infections, C. pneumoniae has also been implicated in chronic respiratory carriage and culture studies have shown that asymptomatic infection may persist for at least a year [Chirgwin et al., 1991; Hyman et al., 1991; Hammerschlag et al., 1992; Hyman et al., 1995]. The seroprevalence of C. pneumoniae IgG antibodies in adults is 50% or more [Wong et al., 1999] but as there is no evidence to suggest that any particular IgG titre can distinguish between current infection and past exposure, it cannot be assumed that half the adult population is chronically infected. Studies have shown that C. pneumoniae can be isolated from the nasopharynx of up to 4.7% of subjectively healthy subjects [Gnarpe et al., 1991; Hyman et al., 1995; Myashita et al., 2001; ]. Hypothetically, if chronic C. pneumoniae infection were highly endemic, then large epidemics would not be expected because of herd immunity. However, both local and generalised outbreaks of C. pneumoniae infection have been described. Reports of localised outbreaks concern mainly young subjects in institutional surroundings such as students at a boy’s school [Pether, Wang & Grayston, 1989] and conscripts at military garrisons [Kleemola et al., 1988; Ekman et al., 1993]. In one study, 43 of 86 conscripts with respiratory symptoms from a garrison of 1200 were diagnosed as having C. pneumoniae infection on the basis of culture or paired serology [Ekman et al., 1993]. Ten of these 43 subjects had pneumonia and the incidence of C. pneumoniae pneumonia was therefore 0.83%, a sizeable epidemic. It is possible that a significant proportion of these subjects had not previously been exposed to C. pneumoniae and this, together with their close proximity may have resulted in the high attack rate. Rates twice as high as this were found for students in another serological study although their living conditions were not described [Saikku et al., 1985]. Reports of generalised outbreaks of C. pneumoniae infection have been retrospective, based on serology and emanate from Scandinavia. In two studies, an increase in the incidence of ornithosis, a notifiable disease, was investigated for the possibility that these had been caused by C. pneumoniae rather than by C. psittaci [Fryden et al., 1989; Grayston et al., 1989]. In one of these studies [Grayston et al., 1989], the incidence of C. pneumoniae pneumonia for Denmark in 1981 can be calculated to be 0.00084% and this increased to 0.0047% in the epidemic year of 1982. Therefore, although there was an approximate six fold increase in incidence, the absolute number of infections was small even allowing for under reporting; whether this can be termed an epidemic is debatable. Nevertheless, a population based seroprevalence study has implied that C. pneumoniae epidemics are frequent and affect significant numbers of the population [Karvonen et al., 1993]. It was found that periods of low and high prevalence (IgG titre ≥ 16), ranging from 44 to 67%, alternated in an epidemic cycle of approximately 10 years. It is difficult to reconcile these figures, which suggest that 20% of the population are involved, with the much smaller figures found in the other studies. As this study did not attempt to measure seroconversion, it does not provide definitive evidence that large scale epidemics occur.

[YW]

[MEW update at March 2002: A study from Japan, based on serology, suggests that C. pneumoniae might be a cause of non specific interstitial pneumonia [Fujita et al., 2001], but patient numbers were small. For a new review see Hahn et al., 2002].

[Author: Yuk-ki Wong edited MEW]

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References

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