Infectious Diseases of the Heart: Pathophysiology, Clinical and Imaging Overview.

Myriad infectious organisms can infect the endocardium, myocardium, and pericardium, including bacteria, fungi, parasites, and viruses. Significant cardiac infections are rare in the general population but are associated with high morbidity and mortality as well as increased risk in certain populations, such as the elderly, those undergoing cardiac instrumentation, and intravenous drug abusers. Diagnostic imaging of cardiac infections plays an important role despite its variable sensitivity and specificity, which are due in part to the nonspecific manifestations of the central inflammatory process of infection and the time of onset with respect to the time of imaging. The primary imaging modality remains echocardiography. However, cardiac computed tomography and magnetic resonance (MR) imaging have emerged as the modalities of choice wherever available, especially for diagnosis of complex infectious complications including abscesses, infected prosthetic material, central lines and instruments, and the cryptic manifestations of viral and parasitic diseases. MR imaging can provide functional, morphologic, and prognostic value in a single examination by allowing characterization of inflammatory changes from the acute to chronic stages, including edema and the patterns and extent of delayed gadolinium enhancement. We review the heterogeneous and diverse group of cardiac infections based on their site of primary cardiac involvement with emphasis on their cross-sectional imaging manifestations. Online supplemental material is available for this article. (©)RSNA, 2016.

Lack of long-lasting hydrosalpinx in A/J mice correlates with rapid but transient chlamydial ascension and neutrophil recruitment in the oviduct following intravaginal inoculation with Chlamydia muridarum.

Lower genital tract infection with Chlamydia trachomatis and C. muridarum can induce long-lasting hydrosalpinx in the upper genital tract of women and female mice, respectively. However, A/J mice were highly resistant to induction of long-lasting hydrosalpinx by C. muridarum. We further compared host inflammatory responses and chlamydial infection courses between the hydrosalpinx-resistant A/J mice and CBA/J mice known to be susceptible to hydrosalpinx induction. Both mouse strains developed robust pyosalpinx during the acute phase followed by hydrosalpinx during the chronic phase. However, the hydrosalpinges disappeared in A/J mice by day 60 after infection, suggesting that some early hydrosalpinges are reversible. Although the overall inflammatory responses were indistinguishable between CBA/J and A/J mice, we found significantly more neutrophils in oviduct lumen of A/J mice on days 7 and 10, which correlated with a rapid but transient oviduct invasion by C. muridarum with a peak infection on day 7. In contrast, CBA/J mice developed a delayed and extensive oviduct infection. These comparisons have revealed an important role of the interactions of oviduct infection with inflammatory responses in chlamydial induction of long-lasting hydrosalpinx, suggesting that a rapid but transient invasion of oviduct by chlamydial organisms can prevent the development of the long-lasting hydrosalpinges.