Chapter 12 : spp.

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The genus spp. consists of highly specialized prokaryotic bacteria that exhibit a unique biphasic developmental cycle that ensures their survival. Along with it is probably the most common cause of community-acquired pneumonia in school-aged children and young adults. This agent has been implicated in the development or acceleration of atherosclerosis, asthma, and chronic obstructive pulmonary disease, and recently, it has been linked to Alzheimer's disease (AD) as well. Recent studies using transmission electron microscopy reveal morphologically atypical chlamydial forms in sites of chronic tissue pathology in vivo, concurrent with reverse transcription (RT)-PCR detection of chlamydial rRNA and mRNA transcripts. Although productive chlamydial infection is the norm, multiple studies suggest the presence of nonculturable persistent chlamydial organisms in host tissues. More importantly, these persistent forms are often found in sites of chronic disease. Several studies report the delayed appearance and prolonged carriage of genital tract strains acquired perinatally. The fact that all species and strains of chlamydiae produce productive infection of appropriate host cells is evidence of their ability to evade phagosome-lysosome fusion. The persistence of chlamydia-specific IgA antibodies has been proposed as a better marker of chronic infections, and of chronic infections as well. Perhaps studies that look at IgA levels in patients with chronic disease in conjunction with immuno-electron microscopy and molecular biological investigations of the patients' tissues would help to confirm both methodologies.

Citation: Darville T. 2000. spp., p 229-261. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch12

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Image of FIGURE 1

Model for the vesicular interactions of the chlamydial inclusion. By 2 h postinfection, in a process that requires early protein synthesis, endocytosed EBs transform the properties of the endocytic vesicles such that they no longer interact with endocytic pathways but begin to intercept sphingolipids from an exocytic pathway. Fluid phase markers or markers for early and later endosomes or lysosomes are not associated with the chlamydial inclusion. Instead, the chlamydial inclusion fuses with a subset o f sphingomyelin-containing vesicles in transit to the plasma membrane. Fusion o f these vesicles exposes the sphingomyelin on the luminal surface of the inclusion membrane, from which it is adsorbed by the chlamydial RBs and incorporated into their cell walls. (Reprinted from reference with permission.)

Citation: Darville T. 2000. spp., p 229-261. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch12
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Image of FIGURE 2

Ultrastructural analysis by electron microscopy of untreated (A) and IFN-γ-treated (B) cells 48 h after infection. Note the typical RB and EB forms in inclusions of untreated cells. The IFN-γ-treated cells do not contain typical chlamydial forms; instead, large atypical RB forms characterize the inclusions. (Photomicrographs provided by Gerald I. Byrne.)

Citation: Darville T. 2000. spp., p 229-261. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch12
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Image of FIGURE 3

Ultrastructural analysis by electron microscopy of rescue of infectious chlamydial forms from cells treated with IFN-γ for 48 h after infection and subsequently cultured in the absence of IFN-γ. At 12 h following the removal of IFN-γ, budding from enlarged RBs (A) was observed. By 24 h following the removal of IFN-γ, nucleoid-like structures were observed within aberrant forms (B). Bar, 1 μm. (Reprinted from reference with permission.)

Citation: Darville T. 2000. spp., p 229-261. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch12
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Image of FIGURE 4

Immuno-electron microscopy of BrdU incorporation during the recovery process. At 24 h after removal of IFN-γ, anti-BrdU antibodies localized DNA synthesis to dense nucleoid masses. (Reprinted from reference with permission.)

Citation: Darville T. 2000. spp., p 229-261. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch12
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