via another source--not sure exactly where

[Guest guest]

Cystic fibrosis, pregnancy, and new acquisition of Burkholderia cepacia

, M.D.

EM is a 37 year old white female with a history of cystic fibrosis who

presented to UNC during her third pregnancy. She had done well with her first

two pregnancies but during the thirty-seventh week of this pregnancy she

developed a cough, productive sputum and high temperatures. She was admitted to

the

hospital for IV antibiotics, subsequently grew Pseudomonas aeruginosa and was

sent home in improved condition to complete a two-week course of antibiotics.

Unfortunately, she returned two days after discharge with return of high

temperatures, increasing purulent cough, and new hemoptysis. Delivery of the

child

was induced, but she continued to have purulent sputum and progression of her

illness. During this hospitalization, her sputum cultures grew Burkholderia

cepacia for the first time. Her antibiotic regimen was changed and she

subsequently improved. Her long-term course has been one of steady decline since

the

original diagnosis. This case, therefore, raises questions regarding the risks

of pregnancy in CF, and whether pregnancy induces immune deficits that may

predispose a CF patient to worsened/new infections. These issues are important

to

address, given the rising number of CF patients who become pregnant each

year.

Over the last eight years, there have been 1091 pregnancies with 551 live

births reported to the CF registry (1). There have been multiple studies done to

evaluate if pregnancy affects pulmonary function and/or mortality; the most

recent and thorough study released in July 2000. This study concluded that

pregnancy did not affect survival or the pulmonary function when compared to

matched, non-pregnant CF controls. Therefore, pregnancy in and of itself may not

pose a significant risk to CF patients unless they have advanced lung disease

(FEV1 <50%) (2). The other question raised by the new acquisition of B. cepacia

during/after pregnancy is whether host immune function declines, and therefore

predisposes patients to infection during this period. Review of the literature

concerning pregnancy and immune function reveals agreement that there may be

down-regulation of T helper type-1 lymphocytes, which may indeed cause an

increase risk for cell-mediated infections (viruses, e.g.). There is no

evidence,

however, that pregnancy may predispose to bacterial infections via this

mechanism (3). It is doubtful, then, that pregnancy predisposed this patient to

the

acquisition of B. cepacia, and that acquisition may have been coincidental,

given lack of evidence or nosocomial acquisition, after a thorough search.

Bibilography

1 CF Registry Data 1991-1998

2 Gilljam, M. et.al, Pregnancy in Cystic Fibrosis; Chest (118): 85-91

3 " Immunology of Pregnancy " , Silver, RM. et.al, Maternal-Fetal Medicine, W.B.

Saunders Company: 72-89