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Many infections in pregnancy have little effect on maternal health, and may result in minimal or no maternal symptoms unless the mother is immunocompromised.
Acute maternal infection can have significant consequences on the mother right through pregnancy because of immunological adjustments.
However certain infections are known to be teratogenic to the developing foetus, and this damage is determined by the gestational age at exposure to infection.
Pregnancy alters the maternal immune system to allow the genetically foreign foetus to develop without causing rejection in a variety of ways.
T helper cells produce cytokines in response to infection.
T helper cells can be further subdivided as:
type 1 T helper cells produce interferon, interleukin, and tumour necrosis factor, which promote an antibody response;
whilst type 2 helper cells produce differing ILs which stimulate a cell-mediated innate immune response.
Cytotoxic T cells kill the pathogens directly.
There is a shift of T helper cells from type 1 to type 2.
Therefore, the antibody-mediated immune response is suppressed, and this is compensated by an increased activation of the innate immune system.
The innate system is less efficient in clearing viruses and bacteria than the specific antibody response.
Hence the pregnant woman is at an increased risk of certain pathogens: some intracellular viruses, bacteria, and parasites.
There is an increased susceptibility of infection to the following pathogens:
Malaria
Measles
Toxoplasmosis
Listeriosis
Leprosy
Pneumocystis carinii
Some pathogens result in an increased severity of disease in pregnancy:
Influenza
Varicella
Psittacosis
Viral haemorrhagic fever (Ebola and Lassa)
Adipose tissue is known to have endocrine, steroidogenesis, and immunological function. Although the full extent of dysregulation of the immune system is not fully understood, and nor is the compounding effect of being pregnant, the following mechanisms have been postulated:
Suppression of functionality of both CD4 T cells and CD8 T cells
T cell diversity
Impaired NK cells
Decreased cytokine production
Lower levels of CD8 and NK cells may account for the increased susceptibility of pregnant obese women to severe illness or mortality from the H1N1 influenza epidemic in 2009.
Obesity is a state of chronic systemic inflammation associated with oxidative stress and with higher baseline levels of inflammatory cytokines and monocytes.
It has been postulated that this chronic inflammatory state may desensitise the response of the immune system and may subsequently diminish the ability to mount an acute cytokine response to an infection.
Oxidative stress in obesity results in an increased proliferation of B cells at the expense of T cells.
Increased B cells levels should be protective against previously encountered pathogens, but obesity has been shown to change the memory T cell response causing individuals to be at a risk of repeat infections.
IgG and IgM negative=absence of infection or extremely recent acute infection.
IgG positive, IgM negative=indicative of previous infection.
IgM (+/– IgG) positive=indicative of current infection (though not in all cases).
IgM and IgG positive=indicative of recent infection or a false-positive test result.
It is recommended that the test may be repeated 2–3 weeks later, and a fourfold rise in IgG antibody titre indicates recent infection.
IgG antibodies can cross the placenta.
NICE guidance screening and treatment for asymptomatic bacteriuria as the risk of ascending infection and consequent risk of pyelonephritis is significant (up to 40%).
17%–20% women report urinary tract infection (UTI) symptoms with symptomatic bacteriuria in pregnancy.
2%–9% of pregnant women have bacteriuria in the first trimester and 10%–30% go on to develop ascending infection in the second or third trimester.
E. coli is thought to be the most common organism, as a bowel commensal. UTIs should be treated to reduce maternal morbidity.
UTIs treatment also reduces risks, including prematurity, as infection can be a trigger for the initiation of labour at any gestation.
Appropriate antibiotics course of 7 days is generally recommended depending upon result of urine culture sensitivity and local antibiotic protocol.
A test of cure repeat urine culture should be carried out 7 days after completion of treatment, especially in women with symptomatic bacteriuria.
It is advisable to avoid Nitrofurantoin in the third trimester due to the risk of haemolytic anaemia,
Trimethoprim should be avoided in the first trimester due to its antifolate effect.
Group B streptococcus (GBS) is the commonest cause of severe early onset infection in the newborn.
Intrapartum antibiotics reduce the incidence of early onset GBS.
Antibiotics treatment have no impact on late onset (after 7 days) which is not associated with maternal GBS.
There is no universal agreement whether routine antenatal screening for GBS should be offered or not, and policy differ globally.
GBS positive bacteriuria should be treated antenatally
Intrapartum antibiotics should be given to women in the following groups:
GBS UTI is identified in pregnancy;
GBS identified on low vaginal and/or anorectal swab during current pregnancy;
had a previous baby affected by GBS.
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