Intrapartum Infections

Objectives

As you complete this module, you will learn:

Risk factors for chorioamnionitis
Effects of chorioamnionitis on uterine contractions and labor progress
Management of chorioamnionitis
Potential perinatal consequences of chorioamnionitis
Group B Streptococcus (GBS) perinatal transmission and potential neonatal consequences of GBS
Screening, diagnosis, and antibiotic management for GBS
Procedure for obtaining GBS cultures
The definition and phases of HIV infection
Common opportunistic infections in those infected with HIV
The state of the HIV/AIDS epidemic
Risk factors for HIV infection
Methods of HIV transmission
Screening and diagnosis of HIV infection
Effects of pregnancy on HIV and HIV on pregnancy, and methods to minimize risk of perinatal transmission
Pharmacotherapeutic treatment recommendations during pregnancy and potential side effects of antiretroviral (ARV) medications
Intrapartum and immediate postpartum management of the HIV-infected mother and newborn
Psychosocial and ethical issues in the care of the HIV-infected mother
Education of the HIV-infected mother
Epidemiology, clinical features, perinatal consequences, and treatments for sexually transmitted infections.

Key Terms

When you have completed this module, you should be able to recall the meaning of the following terms. You should also be able to use the terms when consulting with other health professionals. The terms are defined in this module or in the glossary at the end of this book.

amnion
acquired immunodeficiency syndrome (AIDS)
antibody
antigen
ARV therapy
CD4 cell
chorioamnionitis
chorion
fetal inflammatory response syndrome (FIRS)
funisitis
group B Streptococcus (GBS)
human immunodeficiency virus (HIV)
horizontal transmission
immunoassay
lactobacilli
leukocytosis
opportunistic infection
opt-out HIV screening
perinatal transmission
protease inhibitor
seroconversion
transplacental transmission
vertical transmission
viral load
viral suppression
zidovudine

Part 1 Chorioamnionitis

SUZANNE McMURTRY BAIRD

Introduction

Chorioamnionitis (intra-amniotic infection, amnionitis) occurs in approximately 1% to 10% of all term pregnancies, but approaches 40% to 70% in women with preterm labor (PTL) and birth.¹^,² Risk factors include the following¹^,³:

Psychosocial factors
- Young age (<21 years old)
- Low socioeconomic status
- Alcohol use
- Smoking
Neuraxial anesthesia⁴
Prolonged labor
- Active labor >12 hours⁵
- Second stage of labor >2 hours⁴
Prolonged rupture of membranes (>18 hours)⁴
Multiple cervical exams during labor in women with ruptured membranes
Pre-existing infections of the lower genital tract
GBS bacteriuria
Internal fetal and/or uterine monitoring

NOTE: Combination of risk factors increases the likelihood of infection.

Chorioamnionitis is a broad term that includes any acute, bacterial infection of the chorion (outer fetal membrane), amnion (encloses the fetus), placenta, or the amniotic fluid.³ The most common causative organisms are Escherichia coli, anaerobic gram-positive cocci, GBS, and genital mycoplasmas.¹^,³ These organisms can enter the amniotic membranes/fluid from maternal dissemination, invasive procedures (amniocentesis), but more likely ascend from the vaginal flora when the fetal membranes are ruptured. With less frequency, the inflammatory process of chorioamnionitis can occur with intact membranes and is usually due to genital mycoplasmas such as Ureaplasma species and Mycoplasma hominis, found in the lower genital tract of over 70% of women.⁶

The diagnosis of chorioamnionitis is based on the clinical signs and symptoms—clinical chorioamnionitis. Initial signs and symptoms are maternal fever (temperature >100.4°F) and tachycardia in both the mother (>100/min) and fetus (>60/min for 10 minutes or more). As the infection progresses, other abnormal assessment parameters may include uterine tenderness and purulent, foul-smelling amniotic fluid.¹^,³ Diagnosis is made based on clinical findings, in the absence of other infections of the urinary tract, respiratory system, appendix, or a viral syndrome.¹ Other diagnostic screening may be helpful in the preterm woman in order to determine the need for tocolysis and corticosteroids. The provider may determine the need to perform a transabdominal amniocentesis and directly test the amniotic fluid for infection. Laboratory assessments are listed in Table 12.1.

TABLE 12.1 LABORATORY TESTS FOR CHORIOAMNIONITIS

TEST	SOURCE	ABNORMAL FINDING	NOTE
WBC count	Maternal serum	≥15,000 cells/mm³	Labor and/or corticosteroids may also increase WBC count.
WBC differential	Maternal serum	Leukocytosis (occurs in 70–90% of clinical chorioamnionitis cases) Left shift Bandemia	Isolated leukocytosis may occur in labor and with steroid administration
Glucose	Amniotic fluid	≤10–15%	Excellent correlation with clinical infection and positive amniotic fluid culture
Interleukin-6	Amniotic fluid	≥7.9 ng/mL	Excellent correlation with clinical infection and positive amniotic fluid culture
Leukocyte esterase	Amniotic fluid	>1 + reaction	Good correlation with clinical infection and positive amniotic fluid culture
Gram stain	Amniotic fluid	Any organism	Can identify GBS, but not mycoplasmas
Culture	Amniotic fluid	Growth of aerobic or anaerobic microorganism	Requires incubation time; final results in 3 d.
Blood cultures	Maternal serum; two peripheral sites required	Growth of aerobic or anaerobic microorganism	Positive in 5–10% of patients; requires incubation time; treatment based on clinical diagnosis and should not wait on cultures.
From Duff, P. (2012). Maternal and perinatal infection–bacterial. In Gabbe, S. G., Niebyl, J. R., Simpson, J. L., et al. (Eds.), Obstetrics: Normal and problem pregnancies (6th ed., pp. 1140–115). Philadelphia, PA: Saunders; Tita, A. T., Andrews, W. W. (2010). Diagnosis and management of clinical chorioamnionitis. Clinical Perinatology, 37(2), 339–354.

Maternal fever may occur in a woman with neuraxial anesthesia—“epidural fever”—making it difficult to determine a diagnosis of clinical chorioamnionitis. In addition, neuraxial anesthesia rates are higher in nulliparous women, prolonged labor, and decrease the nurse’s ability to assess uterine tenderness. Medications (ephedrine, neo-synephrine) given for hypotension associated with neuraxial anesthesia also increase the maternal and fetal heart rates. The exact physiologic mechanism of “epidural fever” is unknown. It is theorized that medications used for neuraxial anesthesia block the thermoregulatory processes. However, there is some evidence that suggests higher incidence in the presence of placental inflammation.⁷

NOTE: It is not the nurse’s responsibility to diagnose chorioamnionitis. If the woman becomes febrile or maternal or fetal tachycardia is assessed, notify the provider.

If chorioamnionitis is suspected or diagnosed in the intrapartum period, the placenta and umbilical cord should be sent for pathological examination. In addition, if there is unexpected newborn compromise, histologic examination of the placenta may reveal a diagnosis of inflammation, even in the absence of maternal or fetal symptoms.

Maternal, fetal, and neonatal complications of chorioamnionitis can result in morbidity and morality. If inadequately or untreated, progression of the disease process can occur and lead to fetal inflammatory response syndrome (FIRS).³^,⁸ (See Fig. 12.1.) FIRS is the immune response in the fetus in response to infection- or injury-mediated release of inflammatory mediators such as interleukins, TNF-alpha, C-reactive protein, etc.¹^,⁸^,⁹ FIRS increases fetal and neonatal morbidity and mortality, including the following¹^,³^,⁸^,⁹:

Preterm labor and birth
Hematologic abnormalities
Endocrine activation
Cardiac dysfunction
Pulmonary injury
Renal dysfunction
Brain injury (cerebral white matter)
Perinatal death

FIGURE 12.1 Chorioamnionitis progression. From Duff, P. (2012). Maternal and perinatal infection–bacterial. In Gabbe, S. G., Niebyl, J. R., Simpson, J. L., et al. (Eds.), Obstetrics: Normal and problem pregnancies (6th ed., pp.1140–115). Philadelphia, PA: Saunders; Tita, A. T., & Andrews, W. W. (2010). Diagnosis and management of clinical chorioamnionitis. Clinical Perinatology, 37(2), 339–354.

Funisitis, inflammation of the umbilical cord, occurs with leukocyte infiltration into the umbilical cord or Wharton’s jelly and may include chorionic vasculitis. Up to 60% of chorioamnionitis cases involve funisitis, but the diagnosis of chorioamnionitis is made in all cases of funisitis (Fig. 12.1).⁹

Maternal complications¹^,³:

Postpartum infections
Sepsis
Maternal death

Neonatal complications¹^,³^,⁸^,⁹:

Stillbirth
Preterm birth
Pneumonia
Bacteremia
Meningitis
Neonatal sepsis
Chronic lung disease
Brain injury leading to neurodevelopmental disabilities

Management of Chorioamnionitis

Early Recognition of Signs and Symptoms

The nurse should provide timely assessments of maternal vital signs and fetal status. Early recognition and communication to the provider regarding abnormal assessment parameters (tachycardia, fever), uterine tenderness, or fetal tachycardia expedites diagnosis and intrapartum treatment.

Antibiotic Administration

Intravenous antibiotics that target the most common causative organisms (E. coli and GBS) improve outcomes for the mother and newborn. Evidence demonstrates decreased duration of maternal fever and hospitalization, neonatal bacteremia, and pneumonia with prompt and adequate intrapartum antibiotic treatment versus treatment after birth. The following are the most tested and recommended antibiotic dosing regimes¹:

Ampicillin 2 g IV every 6 hours OR penicillin 5 million units every 6 hours plus gentamicin 1.5 mg/kg every 8 hours.
If the woman is allergic to penicillin or betalactam antibiotics, clindamycin 900 mg every 8 hours should be given.

Antibiotics are usually discontinued after birth or when the mother has been without fever for 24 hours. The provider will individualize the treatment regime for each woman.

NOTE: Even though many cases of chorioamnionitis are caused by ureaplasma species, there are no data to support the use of additional antimicrobial coverage (macrolide antibiotics) to improve outcomes.³

Labor and Birth

Chorioamnionitis increases the risk of dysfunctional labor requiring oxytocin augmentation in 75% of infected women.¹ Every effort should be made to optimize uterine activity while monitoring the fetal response in labor. Fetal tachycardia occurs in greater than three fourths of all cases, and may decrease baseline variability depending on the rate. Therefore, intermittent fetal scalp stimulation may be done to assess fetal acid–base status.¹ Cesarean birth places the woman at increased risk of postpartum complications for wound infection (up to 8%), pelvic abscess (1%), thromboembolism, increased blood loss, and maternal death. In addition, there is no evidence to show improvements in neonatal outcomes.³

NOTE: In isolation, chorioamnionitis is not an indication for cesarean birth.³

If the woman requires a cesarean birth for obstetric reasons, additional antimicrobial coverage for anaerobic organisms is recommended such as clindamycin (900 mg) or metronidazole (500 mg).¹ Antipyretics (acetaminophen) may be given to reduce maternal symptoms such as fever and tachycardia thereby improving the ability for the nurse to assess fetal status. However, the absence of symptoms due to medication does not mean the newborn will not need the presence of the neonatal team at birth or the possibility of assessment and treatment in the nursery.

Newborn Care

With the potential for newborn compromise, the neonatal team should be present at birth for resuscitation needs. Information regarding the mother’s temperature, fetal heart rate monitoring patterns during labor, and antibiotics given during labor should be provided to the team in order for newborn care planning. All well-appearing newborns born to women diagnosed with chorioamnionitis should undergo limited diagnostic evaluation (without a lumbar puncture) and prophylactic antibiotic therapy.¹⁰

Part 2 Group B Streptococcus Infections in Pregnancy

BETSY BABB KENNEDY

Introduction

GBS is a naturally occurring gram-positive bacteria with several different serotypes, and one of the leading infectious causes of morbidity and mortality among newborns.¹

When clinical signs and symptoms appear within the first 24 hours through week of life, it is referred to as early-onset disease, and when signs and symptoms present after 1 week, usually evident in the first 3 months of life, it is referred to as late-onset disease. Although screening and intrapartum antibiotic prophylaxis treatment recommendations have significantly reduced the incidence of early-onset disease, the rate of maternal colonization remains steady.¹

Terminology

Colonization—The presence of microorganisms in an organ or tissue of the body with or without any pathology. The presence of the organism is determined by culture. A positive culture does not indicate infection, but rather that the individual harbors or carries the organism without adverse consequences. For example, if the organism is obtained from surfaces such as skin, ears, or umbilical cord or from gastric contents in a healthy individual, exposure to the organism and colonization are documented. However, infection is not necessarily present. Women who are colonized with GBS may be asymptomatic.
Infection—The invasion by microorganisms of a body site that is normally considered sterile (e.g., bladder, amniotic fluid, blood, lungs, cerebrospinal fluid), causing disease by local cellular injury, secretion of toxins, and other pathologic mechanisms.
Invasive disease—High bacterial load affecting major body systems and inducing serious pathologic events, such as meningitis and respiratory distress.

NOTE: GBS resides in the gastrointestinal tract of many individuals (men and women) without causing any complications. However, close approximation of the anus to the introitus and urethra facilitates colonization of the vagina and urinary tract with GBS. Antibiotic treatment sufficient to eliminate GBS in the gastrointestinal tract of a colonized individual is not possible. Treatment eradicates the organism or, in instances of heavy colonization, lowers the colony count, for locally colonized or infected sites such as the cervix, vagina, or bladder. Colonization can be (1) transient, (2) intermittent, or (3) persistent. GBS colonization of the maternal genital tract involves the most risk to the newborn because of exposure during the birth process. The management goal for the woman with GBS is to reduce infection risks for both mother and neonate.

Epidemiology¹^,²^,³^,⁴^,⁵

It is estimated that 10% to 30% of all pregnant women are GBS carriers.¹^,²
GBS is a common cause of sepsis, pneumonia, and meningitis in neonates and young infants.
Most neonatal infections occur in the first few days of life (early onset).
Reinfection can occur in a small percentage of neonates, and often this is at a new site.
The lower female genital tract, that is, the lower third of the vagina, the vaginal introitus, and the rectum are the most common sites of colonization. The upper third of the vagina and
cervix are less commonly colonized. The urethra can be colonized, leading to urinary tract involvement.
Colonization of the lower maternal genital tract may lead to chorioamnionitis, postpartum endometritis, and neonatal infection.
GBS is a common cause of bacteremia from a urinary tract infection in pregnant women. This can be asymptomatic in a small percentage of women and can lead to pyelonephritis if untreated.
GBS is among the most common causes of intrapartal acute chorioamnionitis.

Early-onset GBS infection is caused by vertical transmission whereby the organism invades the amniotic membranes and infects the fetus in utero. Many newborns are infected before birth.
Although perhaps half of newborns are exposed to GBS when membranes rupture or during the birth process, only a small percentage (1% to 2%) develops the disease.

Maternal risk factors associated with early-onset newborn disease include a positive vaginal/rectal culture, prolonged rupture of membranes, gestational age before 37 weeks’ gestation, intra-amniotic infection, young maternal age, black race.²
Heavy maternal colonization and having an previously given birth to a GBS infected infant increase the risk of neonatal infection.²
Maternal risk factors associated with late-onset neonatal infection are thought to be vertical transmission and hospital-acquired infection.⁴

NOTE: When a GBS-positive infant has been identified, isolation of the infant is not recommended. Outbreaks in nurseries do not occur.⁵

Colonization in women can lead to spontaneous abortion, sepsis, stillbirth, preterm premature rupture of membranes (PPROM), preterm birth, and postpartum endometritis.
Most newborns who develop early-onset invasive GBS disease are term infants.
Preterm infants are more susceptible to early-onset infection.
Signs and symptoms of early-onset infection are generally seen within the first 24 to 48 hours of life (even within the first hour) and include septicemia, pneumonia, and meningitis. Respiratory distress is the most common sign. Infants may be lethargic, have labile temperatures, exhibit poor feeding, and have glucose intolerance.
Signs of severe infection include fetal asphyxia (indicating in utero infection), newborn hypotension, accelerating signs of respiratory distress, and persistent pulmonary hypertension. This requires immediate attention.
The case fatality rate of early-onset disease has dropped dramatically due to implementation of universal screening and subsequent treatment to 4% to 6%. Preterm infants have a higher case fatality rate of 20% of 30%.¹
The mortality rate for late-onset disease is 4% to 6%.¹

Screening¹^,²^,³^,⁴

In 2002, the American College of Obstetricians and Gynecologists (ACOG), American Academy of Pediatrics (AAP), the Association of Certified Nurse Midwives (ACNM), and the Centers for Disease Control (CDC) adopted national prevention guidelines, recommending a single strategy for universal antenatal culture based screening at 35 to 37 weeks’ gestation. Updated guidelines from the CDC, AAP, and ACOG continue to support universal screening but have the following key differences¹:

Expanded recommendations on laboratory methods for the identification of GBS
Clarification of the colony-count threshold required for reporting GBS detected in the urine of pregnant women
Updated algorithms for GBS screening and intrapartum chemoprophylaxis for women with PTL or PPROM
A change in the recommended dose of penicillin-G for chemoprophylaxis
Updated prophylaxis regimens for women with penicillin allergy
Revised algorithm for management of newborns with respect to risk for early-onset GBS disease

Updated recommendations include the following:

Continued culture-based screening
- Vaginal and rectal cultures should be performed at 35 to 37 weeks’ gestation on all pregnant women.
- Cultures done earlier in pregnancy do not predict that colonization will be present at birth. All culture-positive women are treated in the intrapartum period. It is NOT recommended to treat antepartum.¹
- Cervical, perianal, perirectal, or perineal cultures are not recommended, and specula should not be used for specimen collection.

NOTE: A GBS-positive urine culture (in any concentration) in the prenatal period indicates heavy colonization and an increased risk for infection or invasive disease. This requires immediate antibiotic treatment.¹

Risk based approach—When culture results are unknown in the intrapartum period, treat all women with a known risk factor.

Any woman with one or more of the following risk factors in the intrapartum period should be considered for antibiotic treatment:

A history of a previous newborn with invasive GBS infection
A history of GBS bacteriuria during the current pregnancy
Delivery predicted to occur before 37 weeks’ gestation
Rupture of membranes for 18 hours or more
Presence of maternal fever of 38°C (100.4°F) or higher

Maternal Treatment¹^,²^,³^,⁴

Intrapartal treatment is targeted for women documented as being GBS positive (by history or antenatal culture) or for women with intrapartal risk factors.
The CDC recommends treatment must be completed at least 4 hours before the birth so that adequate antibiotic levels are reached in serum and amniotic fluid, thus reducing the risk of newborn colonization.

Antibiotics used in GBS treatment (bactericidal) are known to rapidly reach effective levels in amniotic fluid. Therefore, treatment given less than 4 hours before birth is likely beneficial, with reports that as little as 1 to 2 hours of prophylaxis may offer protection for vertical transmission.¹^,³

Intrapartum chemoprophylaxis includes penicillin-G or ampicillin, with clindamycin, vancomycin, or cefazolin as alternatives for women with penicillin allergy.

Recommended regimen	→	Penicillin-G	First dose 5 million units IV, subsequent doses 2.5– 3 million units q4h until birth
Alternative (Penicillin not available)	→	Ampicillin	First dose 2 g IV, subsequent doses 1 g q4h until birth
Penicillin-allergic (high risk for anaphylaxis)	→	Clindamycin	900 mg IV q8h until birth
Penicillin-allergic (high risk for anaphylaxis, susceptibility unknown)	→	Vancomycin	1 g IV q12h until birth
Penicillin-allergic (low risk for anaphylaxis)	→	Cefazolin	First dose 2 g IV, subsequent doses 1 g q8h until birth

Antibiotic prophylaxis is not indicated in women undergoing a planned cesarean birth in the absence of labor or ruptured membranes due to the low incidence of acquiring disease, but the woman should still have cultures completed at 35 to 37 weeks’ gestation due to the possibility of PPROM and labor beginning prior to the schedule cesarean.

There is currently no alternative oral or intramuscular regimen that is recommended for prophylaxis.¹^,²

Obstetric procedures such as cervical exams and internal electronic fetal and uterine monitoring should not be avoided solely on the basis of positive GBS status.¹^,²^,⁵

Onset of Labor or ROM before 37 Weeks’ Gestation⁴

The preterm infant is at significantly higher risk for GBS sepsis.
If maternal GBS status is negative (in the previous 5 weeks), no antibiotic prophylaxis is needed.
If maternal GBS status is known and positive, antibiotic prophylaxis should be started and continued for at least 48 hours during tocolysis and during labor.
If maternal GBS status is unknown or there has been no culture in the previous 5 weeks, a rectovaginal culture should be obtained. Antibiotic prophylaxis should be started, but may be discontinued when negative results are confirmed or if it is determined the woman is NOT in labor.
If the woman has a GBS culture that is negative at the time of threatened preterm delivery, but does not deliver, repeat cultures should be done again at 35 to 37 weeks’ gestation or upon repeated admission if the prior cultures were completed more than 5 weeks prior.
In the case of PPROM, if antibiotics are being given for latency, that include ampicillin 2 g intravenously (IV) once, followed by 1 g IV every 6 hours for at least 48 hours are adequate for GBS prophylaxis. If other regimens are used, GBS prophylaxis should be initiated in addition.
GBS prophylaxis should be discontinued at 48 hours for women with PPROM who are not in labor. If results from an admission GBS culture become available during the 48-hour period and are negative, GBS prophylaxis should be discontinued at that time.
If the woman with PPROM begins labor and previous culture were done more than 5 weeks previous, she should be rescreened and managed accordingly.

Neonatal Treatment³^,⁴

The CDC algorithm for management of the newborn was revised to apply to all newborns, providing recommendations that depend upon clinical appearance of the neonate and
other risk factors (such as maternal chorioamnionitis, adequacy of intrapartum antibiotic prophylaxis if indicated for the mother, gestational age, and duration of membrane rupture). The algorithm was revised to address unnecessary evaluations in well-appearing newborns at relatively low risk for early-onset GBS disease (see Fig. 12.2 and Table 12.2).³

FIGURE 12.2 Algorithm for secondary prevention of early-onset group B streptococcal (GBS) disease among newborns. (With permission from the CDC—http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5910a1.htm?s_cid=rr5910a1_w)

TABLE 12.2 GBS INTRAPARTUM ANTIBIOTIC PROPHYLAXIS

Indications and nonindications for intrapartum antibiotic prophylaxis to prevent early-onset group B streptococcal (GBS) disease
INTRAPARTUM GBS PROPHYLAXIS INDICATED	INTRAPARTUM GBS PROPHYLAXIS NOT INDICATED
Previous infant with invasive GBS disease	Colonization with GBS during a previous pregnancy (unless an indication for GBS prophylaxis is present for current pregnancy)
GBS bacteriuria during any trimester of the current pregnancy	GBS bacteriuria during previous pregnancy (unless an indication for GBS prophylaxis is present for current pregnancy)
Positive GBS vaginal-rectal screening culture in late gestation during current pregnancy	Negative vaginal and rectal GBS screening culture in late gestation during the current pregnancy, regardless of intrapartum risk factors
Unknown GBS status at the onset of labor (culture not done, incomplete, or results unknown) and any of the following: Delivery at <37 wks’ gestation Amniotic membrane rupture ≥18 hrs Intrapartum temperature ≥100.4°F (≥38.0°C) Intrapartum nucleic acid amplification test (NAAT) positive for GBS	Cesarean birth performed before onset of labor on a woman with intact amniotic membranes, regardless of GBS colonization status or gestational age
Intrapartum antibiotic prophylaxis is not indicated in this circumstance if a cesarean birth is performed before onset of labor on a woman with intact amniotic membranes
Optimal timing for prenatal GBS screening is at 35–37 wks’ gestation
If amnionitis is suspected, broad-spectrum antibiotic therapy that includes an agent known to be active against GBS should replace GBS prophylaxis

SKILL UNIT OBTAINING A GBS CULTURE

Step 1	Informed the woman about the testing procedure and rationale for testing
Step 2	Swab the lower vagina (vaginal introitus)	A speculum should not be used for culture collection
Step 3	Swab the rectum by inserting through the anal sphincter	The same swab or a different swab may be used; cervical, perianal, perirectal, or perineal specimens are not acceptable
Step 4	Place the swab(s) into a nonnutritive transport medium	Appropriate transport systems (e.g., Stuart’s or Amies with or without charcoal) are commercially available. GBS isolates can remain viable in transport media for several days at room temperature; however, the recovery of isolates declines over 1–4 d, especially at elevated temperatures, which can lead to false-negative results. When feasible, specimens should be refrigerated before processing
Step 4	Label the specimen	Specimen requisitions should indicate clearly that specimens are for GBS testing
From Centers for Disease Control and Prevention. (2010). Prevention of perinatal group B streptococcal disease. Morbidity and Mortality Weekly Report, 59(RR-10). Retrieved from: http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5910a1.htm?s_cid= rr5910a1_w .

NOTE: A woman may obtain her own culture if appropriately instructed on the procedure.

Part 3 Human Immunodeficiency Virus (HIV) Infection or Acquired Immunodeficiency Syndrome (AIDS)

CYNTHIA F. KRENING

Introduction

HIV is the virus that can lead to acquired immunodeficiency syndrome, or AIDS. Unlike some other viruses, the human body cannot get rid of HIV once infected. The HIV virus destroys the body’s natural immune system over a number of years. It is transmitted primarily through blood and genital fluids, and to newborn infants from infected mothers. A healthy immune system destroys bacteria, parasites, viruses, and molds that it’s exposed to, preventing damaging effects to the human body. The CD4 cell, also known as the T4 cell or T-helper cell, plays an essential role in orchestrating the body’s immune responses. When the HIV virus invades the body, it uses the CD4 cell for replication. With CD4 lymphocytes, HIV replication can cause cell death; while in other cells, such as macrophages, persistent infection can occur, creating hosts for the virus in many cells and tissues. HIV produces cellular immune deficiency characterized by the depletion of helper T lymphocytes (CD4 cells).

Initially, antibodies are produced in reaction to the penetration of HIV in the cells, and there is a balance between the destruction of CD4 cells during HIV replication and the production of new CD4 cells. Over time though, the individual’s immune system is no longer capable of producing enough new CD4 cells to compensate for the loss of those cells to the virus. Declining numbers of CD4 cells result in the progressive decline of the individual’s immune response and the development of opportunistic infections and neoplastic processes. The HIV virus causes AIDS by interacting with a large number of different cells in the body and escaping the host immune response against it. The host reaction against HIV, through neutralizing antibodies and particularly through strong cellular immune responses, can keep the virus suppressed for many years. Long-term survival appears to involve infection with a relatively low-virulence strain that remains sensitive to the immune response.

Phases of HIV Infection

There are three distinct phases of HIV infection: acute infection and seroconversion, asymptomatic infection and AIDS¹.

Acute Infection and Seroconversion

In humans, 4 to 11 days after mucosal entrance of the virus, there is a rapid onset of plasma viremia with widespread dissemination of the virus.¹ Viral load—the amount of HIV in the blood—expressed by the number of virus copies per milliliter of blood is typically very high at this point. The greater the viral load, the more chance that the CD4 cell count will fall as the virus uses CD4 cells to make copies of itself and destroys those cells in the process. With a high
viral load, the risk of transmission of the virus to others is the highest. Symptoms of seroconversion can include fever, flu symptoms, lymphadenopathy, and rash. These symptoms occur in approximately half of all people infected with HIV. Seroconversion can take a few weeks to several months.¹ Eventually, the immune response will begin to bring the amount of virus back down to a stable level. At this point, CD4 counts will begin to increase, but may not return to pre infection levels.

Asymptomatic Infection

During this phase, HIV is still active, but reproduces at very low levels. Those infected will have few or no symptoms at all for a number of years. This is because the immune response against the virus is effective and vigorous. Those on ARV therapy may live with clinical latency for several decades. If not taking ARVs, this period can last up to a decade, but some may progress through this phase faster. During this phase of clinical latency, those with HIV can still transmit it, even if on ARV therapy, although the medications greatly reduce the risk. Near the end of this phase, the viral load again begins to rise, and the CD4 count begins to drop. Symptoms of HIV infection reappear, as the weakened immune system is unable to provide protection.

AIDS

AIDS occurs when the immune system is damaged enough that it’s vulnerable to opportunistic infections and infection-related cancers. In the United States, a CD4 cell count less than 200/μL is also used as a test to indicate AIDS, although some opportunistic infections develop when CD4 cell counts are higher than 200/μL, and some with CD4 counts under 200/μL may remain relatively healthy. A diagnosis of AIDS is also made when one or more opportunistic illnesses are present, regardless of the CD4 count. Many opportunistic infections and conditions are used to mark when HIV infection has progressed to AIDS. All of these infections and conditions are uncommon or mild in immunocompetent persons. When one of these is unusually severe or frequent in a person infected with HIV, and no other causes for immune suppression can be found, AIDS is diagnosed.² Without treatment, those who are diagnosed with AIDS usually survive about 3 years. In the presence of a dangerous opportunistic illness, life expectancy without treatment falls to an average of 1 year.

Opportunistic infections are caused by organisms that a healthy immune system, under normal situations, could easily destroy on its own or manage to overcome with the assistance of medication. However, with HIV infection, the immune system is compromised, and an opportunistic infection can be life threatening. Opportunistic infections are more frequent or more severe because of immunosuppression in those living with HIV infection. Prior to the widespread use of potent combination ARV therapy, opportunistic infections were the primary cause of morbidity and mortality in this population. Since the early 1990s, better strategies for managing acute infections, chemoprophylaxis, and immunizations have improved quality of life and survival rates.³ Table 12.3 outlines the most common opportunistic infections that occur if the woman has HIV infection.

TABLE 12.3 OPPORTUNISTIC INFECTIONS IN HIV

Early in HIV Infection

Thrush
Shingles
Herpes simplex
Pneumococcal pneumonia
Oral hairy leukoplakia
Thrombocytopenic purpura

Late in the Course of HIV Infection

Pneumocystis carinii pneumonia (PCP)
Kaposi sarcoma
Tuberculosis
Toxoplasmosis
Cryptococcosis
Cryptosporidiosis

From COHIS. (2000). AIDS/HIV opportunistic infections [Online]. Retrieved from: www.medvalet.com/index.html .

HIV and AIDS were the first identified in the early 1980s. In the past 30 years, this disease has become the worst international pandemic of the 20th century. At the end of 2012, 35 million people were living with HIV, although the prevalence of this epidemic continues to vary widely around the world.⁵^,⁶ Currently, more than 1.1 million people in the United States are living with HIV infection.⁷ Over the past decade, the annual number of new HIV infections in the United States has remained relatively stable, although the number of people living with HIV has increased due to prolonged survival.⁷ An estimated 15,529 people with an AIDS diagnosis died in the United States in 2010.⁷ The distribution of people living with HIV and AIDS is concentrated in the southern states, urban communities, and is most prevalent in Black/African-American and Hispanic/Latinos.⁸ In 2011, 25% of HIV-infected people in the United States were women, and 20% of new infections were in women.⁹ Almost 85% of new HIV infections in women are attributed to heterosexual contact. Only about one half of women with an HIV diagnosis were receiving treatment for their condition in 2010, and even less had the virus under control.⁹ The number of women with HIV giving birth in the United States increased approximately 30%, from 2000 to 2006. Despite the increase in the number of women infected with HIV giving birth, the estimated number of perinatal HIV infections per year continues to decline. In 2010, 75% of children infected with HIV acquired it perinatally.¹⁰ This reflects a decline in perinatal transmission from the beginning of the epidemic.¹⁰ The number of children newly infected with HIV in 2012 had declined 35% in 3 years.¹⁰

Risk Factors and Transmission

Some of the factors that place women at increased risk for HIV infection include the following:

Lack of knowledge about male partner’s risk factors for HIV
Vaginal or anal sex without a condom
Fear of talking with male partner about need for condom use
Sexually transmitted diseases (STDs) such as gonorrhea and syphilis
History of sexual abuse
Injection drug and other substance use
Sex with Black/African-American or Hispanic/Latino, due to the high prevalence of people living with HIV in African-American and Hispanic/Latino communities⁹

The risk of acquiring HIV varies with the type of exposure, with some carrying a much higher risk of transmission than others.¹¹ See Table 12.4.

Currently, the most common methods of HIV transmission are the following:

Sexual transmission; homosexual and heterosexual
Perinatal transmission
Parenteral transmission; injection drug users¹²

HIV is transmitted through the following¹³:

Blood
Semen
Pre seminal fluid
Rectal fluid
Vaginal secretions
Breast milk

Fluids must come in contact with a mucous membrane or damaged tissue or be directly injected into the bloodstream (from a needle or syringe) for transmission to occur. HIV transmission occurs vertically or horizontally.

TABLE 12.4 HIV TRANSMISSION RISK

Type of Exposure	Risk per 10,000 Exposures
June 2014
The risk of getting HIV varies widely depending on the type of exposure. Some exposures, such as exposure to HIV during a blood transfusion, carry a much higher risk of transmission than other exposures, such as oral sex. For some exposures, risk of transmission, while biologically plausible, is so low that it is not possible to provide a precise number.
Different factors can increase or decrease transmission risk. For example, taking antiretroviral therapy (i.e., medicines for HIV infection) can reduce the risk of an HIV-infected person transmitting the infection to another by as much as 96%¹, and consistent use of condoms reduces the risk of getting or transmitting HIV by about 80%². Using both condoms and antiretroviral therapy reduces the risk of HIV acquisition from sexual exposure by 99.2%³. Conversely, having a sexually transmitted infection or a high level of HIV virus in the blood (which happens in early and late-stage infection) may increase transmission risk.
The table below lists the risk of transmission per 10,000 exposures for various types of exposures.
Estimated Per-Act Probability of Acquiring HIV from an Infected Source, by Exposure Act^*
Parenteral³
Blood Transfusion	9,250
Needle-sharing during injection drug use	63
Percutaneous (needle-stick)	23
Sexual³
Receptive anal intercourse	138
Insertive anal intercourse	11
Receptive penile-vaginal intercourse	8
Insertive penile-vaginal intercourse	4
Receptive oral intercourse	low
Insertive oral intercourse	low
Other†
Biting	negligible⁴
Spitting	negligible
Throwing body fluids (including semen or saliva)	negligible
Sharing sex toys	negligible
Reprinted with permission from the CDC.
^* Factors that may increase the risk of HIV transmission include sexually transmitted diseases, acute and late-stage HIV infection, and high viral load. Factors that may decrease the risk include condom use, male circumcision, antiretroviral treatment, and pre-exposure prophylaxis. None of these factors are accounted for in the estimates presented in the table.
^† HIV transmission through these exposure routes is technically possible but unlikely and not well documented.
¹ Cohen MS, Chen YQ, McCauley M, et al; HPTN 052 Study Team. Prevention of HIV-1 Infection with early antiretroviral therapy. N Engl J Med 2011;365(6):493–505.
² Weller SC, Davis-Beaty K. Condom effectiveness in reducing heterosexual HIV transmission (Review). The Cochrane Collaboration. Wiley and Sons, 2011.
³ Patel P, Borkowf CB, Brooks JT. Et al. Estimating per-act HIV transmission risk: a systematic review. AIDS. 2014. doi: 10.1097/QAD.0000000000000298.
⁴ Pretty LA, Anderson GS, Sweet DJ. Human bites and the risk of human immunodeficiency virus transmission. Am J Forensic Med Pathol 1999;20(3):232–239.

Horizontal Transmission of HIV

In horizontal transmission, the virus is transmitted from an HIV-infected person to another by direct contact. Examples of such contact include the following:

Intimate sexual contact (oral, anal, or vaginal) with someone infected with the HIV.
Sharing of drug needles and syringes with an infected individual.
Receipt of a blood transfusion that contains HIV—Risk from blood transfusions has been virtually eliminated through careful screening procedures now done on all donated blood and plasma.
Inadvertent contamination of mucous membranes or breaks in the skin (e.g., of a nurse or other healthcare provider) by the blood or body fluid of the infected person.

Vertical Transmission of HIV

Vertical transmission of HIV occurs when the virus is passed from the mother to her infant during the perinatal period. Transmission can occur during the antepartum, intrapartum, or postpartum period. HIV has been isolated from many sources (early gestational embryo, blood, breast milk, amniotic fluid, cord blood, and the placenta), which indicates multiple potential routes of fetal or neonatal transmission. The virus has been isolated in 13- to 20-week-old fetuses, but transmission is generally believed to occur most often in late pregnancy.¹⁴^,¹⁵ In the United States, the extensive implementation of the Public Health Service guidelines for
universal counseling and testing, and the use of a combination of ARV agents have sharply reduced transmission risk and the number of mother-to-infant transmissions. Risk factors for vertical transmission include the following:

Immunologically or clinically advanced HIV disease
Increased plasma viral load
Injected drug use during pregnancy
Low CD4 cell count
Breastfeeding
Lack of ARV therapy in pregnancy
Invasive procedures; for example, amniocentesis, fetal scalp electrode, fetal scalp sampling

NOTE: The Public Health Service provides specific management guidelines for postexposure ARV intervention. Every institution should use these guidelines.

Diagnosis of HIV

The antibody screening test (immunoassay) is the most common test for the presence of HIV. It tests for antibodies that the body makes against HIV. The immunoassay may be conducted in a lab or as a rapid test. Most blood-based lab tests find infection sooner after exposure than rapid HIV tests. Other tests can detect both antibodies and antigen (part of the virus itself). These tests identify recent infection earlier than tests that detect only antibodies. As soon as 3 weeks after exposure to the virus, the antigen/antibody combination tests can find HIV in the bloodstream. The rapid test is an immunoassay used for screening, producing quick results, usually within an hour or less. Rapid tests detect HIV antibodies in the blood. If an immunoassay (lab test or rapid test) is conducted during the window period (the period after exposure but before the test can detect antibodies), a false-negative result may be reported.

All immunoassays that are positive require follow-up diagnostic testing to confirm the result. Follow-up tests include the following:

antibody differentiation test, which distinguishes HIV-1 from HIV-2;
HIV-1 nucleic acid test, which looks for virus directly; or the
Western blot or indirect immunofluorescence assay, which detect antibodies.

Although immunoassays are generally very accurate, follow-up testing is routine.¹⁶ The CDC has published updated recommendations for HIV testing by US laboratories. The revised algorithm is a sequence of tests used in combination to improve the accuracy of the laboratory diagnosis of HIV. These updated guidelines include tests for HIV antigens and nucleic acid. Studies have shown that antibody testing alone may miss a considerable percentage of HIV infections detectable by virologic tests.¹⁷

All pregnant women should be offered routine, universal HIV testing early in pregnancy. ACOG, the Institute of Medicine, CDC, other leading professional organizations, and most states support opt-out HIV screening. With this approach to testing, the patient is notified that HIV testing will be performed as a routine part of obstetric care and written consent is not required. As with any testing, the woman has the option to opt out and decline testing. This approach helps to reduce barriers to testing that may result from extensive counseling or from perceptions of stigmatization associated with HIV status. If a woman initially declines testing, education should be provided, and she should continue to be encouraged to be tested. Women with an acute infection who have symptoms of acute retroviral syndrome or who suspect recent HIV exposure should be offered repeat testing. Repeat testing should also be offered during the third trimester of pregnancy to women who had an earlier negative HIV test but who have continued high-risk behaviors. If a woman presents with symptoms of labor and an unknown HIV status, rapid HIV testing should be done (using an opt-out consent strategy when allowed by jurisdiction).¹⁸

Newborns of women who decline HIV testing or whose infection status remains unknown at birth should have rapid antibody testing as soon as possible after birth. The mother should be informed that a positive newborn test indicates maternal HIV infection but not necessarily an infant
infection.¹⁸ Screening all pregnant women for HIV, and giving them appropriate medical care, helped to decrease the number of babies born with HIV from a high of 1,650 in 1991 to 127 in 2011.¹⁶

Even though pregnancy is accompanied by a mildly immunosuppressive state, no conclusive evidence exists that pregnancy aggravates the health of the expectant woman who has HIV infection.¹⁹ Evidence has shown no overall significant differences in HIV disease progression, progression to AIDS, fall in CD4 count to below 200 or death comparing pregnant women and nonpregnant women with HIV infection.²⁰ In addition, there is no difference in viral load, CD4, or progression of clinical disease in women who had one pregnancy when compared with women with more than one pregnancy.²¹

During pregnancy, a decline in absolute CD4 cell counts is seen in both HIV-positive and HIV-negative women. It is thought to be secondary to hemodilution of pregnancy. Therefore, the use of a percentage of CD4 cells, rather than an absolute number of CD4 cells, is the most accurate method to measure immune function. Pregnancy does not accelerate a decline in CD4 cells, and HIV RNA (viral load) levels remain relatively stable during pregnancy.²²

There is some evidence that during the postpartum period viral load levels increase despite ARV therapy, possibly due to immune activation associated with hormonal changes, or the end of pregnancy-related viral load suppression. Transmission risk and treatment recommendations have not been clarified for this increase in viral load.²³^,²⁴^,²⁵ This postpartum increase in viral load does not appear to be long-lasting.²¹^,²⁵

Some studies suggest that HIV-infected women may have multiple coexisting risk factors for adverse pregnancy outcome including sexually transmitted infections (STIs), malnutrition, poverty, substance abuse, domestic violence, and inadequate or no prenatal care. If these problems are controlled for, there is no independent effect of HIV on adverse outcomes.²⁶ Risk factors for adverse pregnancy outcomes in women receiving ARV therapy are similar to those reported in uninfected women.²⁶ There may be a slightly increased risk for preterm delivery prior to 37 weeks’ gestation in women taking protease inhibitors (PIs), but data are conflicting.²⁷ The clear benefits of ARV agents in reducing perinatal transmission of HIV outweigh the conflicting data regarding preterm birth.

Reducing Perinatal Transmission

NOTE: no Therapies Guarantee A 0% Risk Of Vertical Transmission. The Highest Risk for Vertical Transmission is Among Women With Relatively High Plasma Viral Loads.

Every infant that is born HIV infected is a sentinel health event as a result of either a missed prevention opportunity or, rarely, prophylaxis failure.

Strategies to Prevent Transmission

Early prenatal care
Universal HIV testing
In the HIV-positive woman:
- Reducing viral load
- ARV regimen
- Minimizing exposure of fetus to HIV during the intrapartum period
- Preventing exposure to HIV infection during the postpartum period

Transmission rate can be reduced to less than 2% with universal screening of women in combination with ARV prophylaxis, scheduled cesarean birth when indicated, and avoidance of breastfeeding.²⁸

The viral load (also called the HIV RNA test) is a measurement of the magnitude of active HIV replication. The viral load assesses the relative risk for disease progression and the efficacy of ARV therapies. The CD4 cell count is an indicator of the extent of immune system damage. The CD4 cell count assesses the risk for developing specific opportunistic infections and other sequelae of HIV infection. When the viral load and the CD4 cell count are used together, the risk for disease progression can be predicted.

NOTE: The viral load correlates with the risk of perinatal transmission.

Mother-to-child transmission of HIV is the most common way that children become infected with the virus. Although perinatal HIV transmission can occur during pregnancy, labor, and birth, or during breastfeeding, currently the risk of perinatal transmission is less than 2% in the United States and Europe. HIV-infected pregnant women should be educated that ARV drug regimens during pregnancy are highly recommended because viral suppression significantly decreases the risk of transmission to the fetus. Full viral suppression decreases the risk of perinatal HIV transmission to around 1%,²⁹ while those with a viral load greater than 30,000 copies/mL have a transmission rate of up to 23%.³⁰ Unfortunately, data indicate that even some women with an undetectable viral load are still able to transmit the virus to their newborn. Because the low residual risk may be due to the presence of HIV in the genital secretions, ARV prophylaxis is recommended for all pregnant women regardless of their viral load.

The current standard of care is the simultaneous use of three ARV drugs for full viral suppression. In making decisions regarding treatment in a pregnant woman, the following must be considered:

The treatment of HIV infection
Reduction of the risk of perinatal transmission
The known and unknown benefits and risks of therapy as well as nontherapy

Careful medication selection is important to avoid toxicity in the woman and developing fetus. Combination ARV regimens are more effective in reducing transmission than a single-drug regimen. Prophylaxis antepartal, and during the intrapartum and postpartum period, combined with newborn prophylaxis is more effective than only intrapartum and postpartum treatments. The earlier in pregnancy prophylaxis is initiated, the more effective the regimen is in reducing perinatal transmission.

Pregnancy is not a reason to delay standard HIV treatment for maternal health. In 2012, 62% of pregnant women living with HIV were receiving ARV treatment.⁵ Recommended treatments for viral suppression during pregnancy are outlined in Table 12.5.

TABLE 12.5 RECOMMENDED STRATEGIES FOR VIRAL LOAD SUPPRESSION

	PREGNANCY RECOMMENDATIONS
On antiretroviral therapy with viral suppression	Continue antiretroviral medications if tolerating regime Certain agents may require dosing changes
On antiretroviral therapy without viral suppression	Evaluate reason viral suppression has not been achieved (nonadherence, drug resistance) Consider drug resistance testing and new antiretroviral medication regime tailored to the resistance profile and medication tolerance of the woman

NOTE: The standard of care is the simultaneous use of multiple ARV drugs to suppress the viral load below detectable limits regardless of CD4 cell count or plasma HIV RNA copy number, in order to prevent perinatal transmission of HIV.

Treatment Naïve (Treatment in Someone Who Has Never Taken HIV Drugs Before as Opposed to Someone Who Is “Treatment-Experienced”)

Perinatal transmission of HIV is decreased with initiation of an ARV regimen early in pregnancy, so that viral suppression is attained by the time of birth.³¹^,³² However, the benefits of any
medication regimen must be weighed against any known fetal teratogenic effects of drug exposure in the first trimester. In the first trimester of pregnancy, women who have not begun ARV therapy may wish to delay initiation of therapy until after completion of organogenesis at 10 to 12 weeks’ gestation. Delaying initiation of medications until the second trimester is an option if CD4 cell count is greater than 350 cells/μL. ARV prophylaxis should be initiated regardless of gestational age if the CD4 cell count is less than 350 cells/mm,³ symptoms of HIV disease, or a co-infection, a high viral load or AIDS are present.²⁷

Tags: Intrapartum Management Modules: A Perinatal Education Program

Nov 6, 2018 | Posted by drzezo in GYNECOLOGY | Comments Off

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