Coccidioidomycosis in Pregnancy: Case Report and Review of the Literature

Crum, Nancy F.; Ballon-Landa, Gonzalo

doi:10.1016/j.amjmed.2006.04.022

Cited by 44 publications

(37 citation statements)

References 24 publications

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“…Although pregnancy does not increase the risk of coccidioidomycosis, it has been critically linked with disseminated disease, especially during the third trimester and the postpartum period [62]. In a review of 29 cases of coccidioidomycosis that occurred during the third trimester of pregnancy, the mortality rate was 55%, and among 7 cases that occurred during the postpartum period, the mortality rate was 29% [63].…”

Section: Fungimentioning

confidence: 98%

Immune Reconstitution Syndrome and Exacerbation of Infections after Pregnancy

Singh

Perfect

2007

Clinical Infectious Diseases

169

143

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Pregnancy is a state of subtle immunosuppression characterized by physiologic suppression of proinflammatory host responses that are meant to promote embryonic implantation. Rapid reversal of these changes and a rebound of inflammatory responses during the postpartum period can result in quiescent or latent infection manifesting as symptomatic disease. Infections due to several microbial pathogens and noninfectious diseases with an autoimmune basis have been shown to worsen or begin during the postpartum period. Awareness that symptoms resulting from immune reconstitution can occur in any host with a rapidly changing immunologic repertoire, including women in the postpartum phase, is a critical first step in fully understanding this phenomenon. Future studies to discern the precise pathophysiologic basis of immune reconstitution, to identify pregnant women at risk, and to determine markers that may be diagnostically helpful have significant implications for optimizing treatment of these patients.

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Section: Fungimentioning

confidence: 98%

Immune Reconstitution Syndrome and Exacerbation of Infections after Pregnancy

Singh

Perfect

2007

Clinical Infectious Diseases

169

143

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“…Pregnant women are especially vulnerable to coccidioidal infection, and their risk of developing severe or disseminated disease rises when infection is acquired in the later stages of pregnancy 74,75. Also, severe coccidioidomycosis is more likely to occur during the immediate postpartum period if infection is acquired in the third trimester 74,76.…”

Section: Risk Factors For Infectionmentioning

confidence: 99%

“…Two retrospective reviews of Kern County birth records from the 1940s to the 1960s were notable for a rate of 7.7–11 coccidioidomycosis cases per 10,000 pregnancies, with a striking rate of death (33%) among women who had disseminated disease 77,78. A more recent review of 81 coccidioidomycosis cases in pregnant women found that disseminated disease occurred in 50% of the cases diagnosed in the first trimester, 62% in the second trimester, and 96% in the third trimester 75. These extremely high rates of dissemination, which have not been seen in other investigations, may reflect a component of reporting bias.…”

Section: Risk Factors For Infectionmentioning

confidence: 99%

Coccidioidomycosis: epidemiology

Thompson¹,

Brown²,

Benedict³

et al. 2013

CLEP

144

106

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Coccidioidomycosis consists of a spectrum of disease, ranging from a mild, self-limited, febrile illness to severe, life-threatening infection. It is caused by the soil-dwelling fungi, Coccidioides immitis and C. posadasii, which are present in diverse endemic areas. Climate changes and environmental factors affect the Coccidioides lifecycle and influence infection rates. The incidence of coccidioidomycosis has risen substantially over the past two decades. The vast majority of Coccidioides infections occur in the endemic zones, such as California, Arizona, Mexico, and Central America. Infections occurring outside those zones appear to be increasingly common, and pose unique clinical and public health challenges. It has long been known that elderly persons, pregnant women, and members of certain ethnic groups are at risk for severe or disseminated coccidioidomycosis. In recent years, it has become evident that persons with immunodeficiency diseases, diabetics, transplant recipients, and prisoners are also particularly vulnerable.

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“…Whether symptomatic or not, most immunologically intact people recover spontaneously from the primary infection, but ϳ5% of infections spread to extrathoracic sites, and these do not resolve spontaneously. Immunosuppression (4,5), including the immunological changes that occur in the third trimester of pregnancy (6), is a risk factor for dissemination of infection, but disseminated infections can occur in previously healthy individuals with no known immune defects (7). Little is known about the risk factors for dissemination in normal hosts, but genetic factors are important, since African Americans and Filipinos are 5 to 10 times more likely than Caucasians to develop disseminated infections (8)(9)(10).…”

mentioning

confidence: 99%

Neither Dectin-2 nor the Mannose Receptor Is Required for Resistance to Coccidioides immitis in Mice

et al. 2014

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We investigated the roles of the mannose receptor (MR) and Dectin-2 in resistance to pulmonary coccidioidomycosis in C57BL/6 (B6) mice and in the interaction of myeloid cells with spherules, using B6 mice with targeted mutations in Mrc1 and Clec4n. Spherules are the tissue form of Coccidioides, and we determined that the MR on bone marrow-derived dendritic cells (BMDC) was important for recognition of spherules (formalin-killed spherules [FKS]) and for secretion of interleukin 10 (IL-10) and proinflammatory cytokines in response to FKS by both elicited macrophages and BMDC. Infected MR knockout (KO) mice produced more IL-10 in their lungs than did B6 mice, and MR KO mice also made more protective Th-17 cytokines. In contrast to the MR, Dectin-2 was not required for recognition of FKS by BMDC or for the production of cytokines by BMDC in response to FKS. However, Dectin-2 KO was required for stimulation of elicited peritoneal macrophages. Despite that, lung cytokine levels were not significantly different in Dectin-2 KO mice and B6 mice 14 days after infection, except for IL-1␤, which was higher in Dectin-2 KO lungs. Although both Dectin-2 ؊/؊ and MR ؊/؊ myeloid cells had reduced proinflammatory cytokine responses to FKS in vitro, neither MR nor Dectin-2 deficiency reduced the resistance of B6 mice to pulmonary coccidioidomycosis.

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Coccidioidomycosis in Pregnancy: Case Report and Review of the Literature

Cited by 44 publications

References 24 publications

Immune Reconstitution Syndrome and Exacerbation of Infections after Pregnancy

Immune Reconstitution Syndrome and Exacerbation of Infections after Pregnancy

Coccidioidomycosis: epidemiology

Neither Dectin-2 nor the Mannose Receptor Is Required for Resistance to Coccidioides immitis in Mice

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