1. Sexually transmitted diseases 2. Tuberculosis
3. Endocarditis
Enterococcal Infections
The genusEnterococcusincludes all the members that were previously classified with group DStreptococci.2
These organisms are gram-positive cocci which are the normal residents of the gastrointestinal tract and biliary tract and in lower numbers are known to colonise the vagina and male urethra.
The organisms under this genus are important because they are increasingly becoming agents of human disease because of their resistance to many antimicrobials to which most Streptococci are susceptible.
Enterococcus species are a component of the human intestinalflora and may be found in the birth canals of women.
They are one of the most common causes for hospital-acquired urinary tract, wound and blood- stream infection. This organism is most commonly isolated from women with post-caesarean endometri- tis and wound infections.
Microbiology of Enterococci
These are a group of gram-positive cocci that have been distinguished from Streptococci based on the following properties:
1. Ability to grow at 10°C and 45°C 2. Growth in presence of 6.5 per cent NaCl 3. Growth at pH 9.6
4. Ability to hydrolyse esculin in presence of 40 per cent bile
5. Production of pyrrolidonyl arylamidase (PYR)
Risk Factors for Enterococcal Bacteraemias
• Advanced age
• Immunosuppression
• Underlying diseases
• Prematurity of baby
• Genitourinary tract instrumentation
• Usage of broad-spectrum antibiotics with little or no enterococcal activity (e.g. cephalosporins)
Common Infections Caused by Enterococci
1. Urinary tract infections (UTIs) and asymptomatic bacteriuria (ASBU)
2. Genitourinary tract infection 3. Neonatal enterococcal sepsis 4. Enterococcal meningitis in neonates
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5. Puerperal sepsis 6. Pneumonia
7. Wound and soft tissue infections
Drug Resistance in Enterococci
• Enterococcidisplay intrinsic, low-level resistance to aminoglycosides and lincosamides.
• They have relatively high minimum inhibitory concentrations (MICs) for penicillin and cephalosporins due to diminished binding of cell wall penicillin-binding proteins (PbP) to these agents.
• They are resistant to the action of sulfonamides in vitro.
• They are still able to block folate synthesis.
• Low-level aminoglycoside resistance is due to decreased penetrability of enterococcal cell wall.
• Serious infections with low-level resistance to aminoglycosides can be treated with
a combination of penicillin/ampicillin with an aminoglycoside.
• High-level aminoglycoside resistance has emerged due to transposons and this is easily transmitted to other organisms.
• High-level aminoglycoside resistance has been documented in various strains likeE. faecalis, E. faecium, E. gallinarum, E. pullorumetc. Such infections cannot be treated with a combination of β-lactam agent and aminoglycoside antibiotic.
• Since the 1980s there has been a huge change in the pattern of susceptibility ofEnterococcito vancomycin and ampicillin, leading to the emergence of vancomycin-resistantEnterococci (VRE).10
Epidemiology of Bacterial Infections in Pregnancy
• In a study conducted by Ettore Cincinelli et al., it was found thatE. faecaliscontributed to
22.9 per cent of positive cultures among patients with endometritis who had miscarriages in the past.
• A study undertaken by S Ahmed et al. on aerobic bacterial pattern puerperal sepsis found that E. faecaliscontributed to 4.76 per cent of the total aerobic isolates isolated from cases of puerperal sepsis.
• According to K Fisher and C Phillips, in the year 2005 in the UK there were a total of 7066 cases of
enterococcal bacteraemias, 63 per cent of which were due toE. faecalisand 28 per cent toE. faecium.
• A study conducted by R Colgan et al. on
asymptomatic bacteriuria in adults observed that healthy persons with ASBU will be likely to be infected with E. coli, whereas a person with indwelling catheter is more likely to be infected with multidrug-resistant organisms like Enterococci.11
• A Cochrane systematic review found that treatment of ASBU in pregnancy decreases the risk of subsequent pyelonephritis from a range of 20–35 per cent to a range of 1–4 per cent.12 [EL 1]
Signs and Symptoms
Signs and symptoms vary according to the site of infection (pneumonia, UTI, endometritis, chorioam- nionitis, endocarditis, puerperal sepsis etc.).
Work-Up in Bacterial Infections
Specimens to be cultured are
• Blood culture
• Serous/purulent discharge from episiotomy wounds
• Swab of purulent drainage
• Tissue biopsy
Maternal Implications of Enterococcus Infection
1. MaternalEnterococcibacteraemia may lead to shock or disseminated intravascular coagulation 2. Enterococcusinfection may lead to endocarditis, especially in pregnant women with cardiac valve prosthesis
3. A common aetiology in UTI during pregnancy 4. Postpartum endometritis
5. Puerperal sepsis 6. Pneumonia
Fetal Implications of Enterococcus Infection
• Intrauterine infection triggers an inflammatory response believed to result in preterm labour (PTL) and injury to the developing fetal lung and brain.
Pro-inflammatory cytokines and chemokines, Section 2: Infections in Pregnancy
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• Intrauterine infection and inflammation is frequently associated with adverse fetal outcomes. In many studies of all preterm births, the incidence of positive amnioticfluid and chorioamniotic culture was as high as 40 per cent. In many cases, infection is largely subclinical.
• Micro-organisms may gain access to the amniotic cavity and fetus through ascending infection from the vagina and cervix; haematogenous
dissemination through the placenta
(transplacental infection); retrograde seeding from the peritoneal cavity through the fallopian tubes; and inadvertent introduction of infective agents at the time of invasive procedures (amniocentesis, percutaneous fetal blood sampling, chorionic villous sampling or shunting).13
BacterialEnterococcusinfection is associated with:
• High perinatal mortality rate
• Low birthweight
• Preterm labour
• Injury to the developing fetal lung and brain
Treatment
Monotherapy
1. Ampicillin is thefirst choice for monotherapy of susceptibleE. faecalisinfection.
2. Vancomycin is used for patients with penicillin allergy or infections with strains that have high- level penicillin resistance.
3. Nitrofurantoin is effective in the treatment of enterococcal UTIs, including many caused by VRE strains.
4. Linezolid, daptomycin or tigecycline may be used to treatE. faeciumandE. faecalisstrains, including VRE.14
Polytherapy
1. Ampicillin, vancomycin and an aminoglycoside (e.g. gentamicin category C) are considered the standard treatment forE. faecalis, particularly in native valve endocarditis. At least four weeks of therapy is recommended. Consideration should be given to limiting the aminoglycoside component
to two weeks in order to avoid nephrotoxic vestibular and ototoxic complications.
2. Ceftriaxone plus ampicillin, given as intravenous ampicillin 2 g every four hours plus intravenous ceftriaxone 2 g every 12 hours.15
Conclusion
Enterococci are gram-positive cocci which normally reside in the gastrointestinal tract and biliary tract and in lower numbers are known to colonise the vagina and male urethra. During pregnancy they may cause serious infections affecting the health of the mother and baby.
Treatment options include either monotherapy of any of these agents (ampicillin, vancomycin, nitrofur- antoin, linezolid, daptomycin or tigecycline) or poly- therapy of a combination of two or more antibiotics.
Bacterial Infection in Food Poisoning
Food-borne bacterial infection can be worse during pregnancy and may lead to miscarriage or premature delivery. It can also lead to death or severe health problems in newborn babies. Some food-borne infec- tions (e.g. Listeria, Toxoplasma gondii, E. coli and Salmonella) can infect the fetus even if the mother does not feel sick.
The commonest pathogens are:
• Listeria
• E. coli
• Salmonella
• Campylobacter
• Toxoplasma gondii
Signs and Symptoms
• Stomach cramps
• Vomiting
• Diarrhoea
Vomiting and diarrhoea may lead to serious dehy- dration and death if not treated properly.
Diagnosis of Food Poisoning
1 History
Eating and travel history may offer a clue to the diagnoses.
2 Clinical Examination
Signs of hydration include dry, tenting skin, sunken eyes, dry mouth, and lack of sweat in the armpits and
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groin. There may be a low-grade fever and low blood pressure.
3 Stool Samples
These may showSalmonella, E. coli or other organisms.
Treatment of Bacterial Food Poisoning
1. Maintaining good hydration is thefirst step.
Hospitalisation is indicated if the patient is dehydrated or if there is clinical or laboratory evidence offluid or electrolyte imbalance in their body.
2. Medications may be prescribed to control nausea and vomiting.
3. Medications to decrease the frequency of diarrhoea may be indicated, e.g. loperamide (Imodium).
4. Antibiotics
Antibiotics are not routinely indicated in cases of food poisoning. Except for specific infections, anti- biotics are not prescribed in the treatment of most food poisoning. Decision should be based on multiple factors (the intensity of the disease symptoms, if there is serious response to infection (sepsis)).
A pregnant woman suspected of having listeriosis will likely be treated with intravenous antibiotics because of the effect of the infection on the fetus.
Prevention of Food Poisoning during Pregnancy
16• Avoid raw and smoked seafood.
• Avoid unpasteurised juice or cider.
• Avoid unpasteurised milk and milk products, which may cause brucellosis.
• Avoid soft cheese.
• Only consume well-cooked eggs, because undercooked eggs may containSalmonella.
• Avoid undercooked meat and poultry.
• Avoid or reheat hot dogs and luncheon meats.
• Be cautious with meat spreads or pâté (risk of Listeriainfection).
• Avoid mercury-containingfish (king mackerel, marlin, shark, swordfish and tilefish).
References
1. Institute of Obstetricians and Gynaecologists, Royal College of Physicians of Ireland and the National Clinical Programme in Obstetrics and Gynaecology.
2015. Clinical Infections Practice guideline; bacterial Infections Specific to Pregnancy.
2. Winn WC Jr, Koneman EW.Koneman’s Color Atlas and Textbook of Diagnostic Microbiology, 6th ed.
Philadelphia: Lippincott Williams; 2006.
3. Tille P.Bailey & Scott’s Diagnostic Microbiology, 13th ed. St Louis, MO: Mosby; 2013.
4. Baron S, Salton MR, Kim KS. Structure. In:
Baron S, Salton MR, Kim KS.Baron’s Medical Microbiology, 4th ed. Galveston: University of Texas Medical Branch; 1996.
5. Higgins RD, Saade G, Polin RA et al., for the Chorioamnionitis Workshop Participants. Evaluation and management of women and newborns with a maternal diagnosis of chorioamnionitis:
summary of a workshop.Obstet Gynecol. 2016;127(3):
426–36.
6. Owens CD, Stoessel K. Surgical site infections:
epidemiology, microbiology and prevention.J Hosp Infect.2008;70(suppl 2): 3–10.
7. Sharma RK, Parashar A. The management of perineal wounds.Indian J Plast Surg. 2012;45(2): 352–63.
8. Goodnight WH, Soper DE. Pneumonia in pregnancy.
Crit Care Med. 2005;33(suppl 10): S390–7.
9. American College of Obstetricians and Gynecologists. Listeria and Pregnancy. PFS013, January 2017.www.acog.org/Patients/FAQs/Listeria- and-Pregnancy.
10. Miller, WR, Munita JM, Arias CA. Mechanisms of antibiotic resistance in enterococci.Expert Rev Anti Infect Ther. 2014;12(10): 1221–36.
11. Cormican M, Murphy AW. Akke Vellinga.
Interpreting asymptomatic bacteriuria.BMJ. 2011;
343: d4780.
12. Smaill FM, Vazquez JC. Antibiotics for bacterial infection in the urine in pregnancy when there are no symptoms. 2015 Cochrane review.
13. Adams Waldorf KM, McAdams, RM. Influence of infection during pregnancy on fetal development.
Reproduction.2013;146(5): R151–62.
14. Plosker GL, Figgitt DP. Linezolid:
a pharmacoeconomic review of its use in serious Gram-positive infections.Pharmacoeconomics. 2005;
23(9): 945–64.
15. Kristich CJ, Rice, LB, Arias CA. Enterococcal Infection–Treatment and Antibiotic Resistance. 2014.
www.ncbi.nlm.nih.gov/books/NBK190424/.
16. US Department of Health and Human Services. Food Safety for Pregnant Women. 2017.www.fda.gov/food/
foodborneillnesscontaminants/peopleatrisk/uc m312704.htm.
Section 2: Infections in Pregnancy
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20 Listeriosis
Adel Elkady, Prabha Sinha and Soad Ali Zaki Hassan
Prevalence and Incidence
In the general population, Listeriainfection is rela- tively uncommon, with a prevalence of approximately 4 per million in Canada, 0.27 per million in the USA and between 0.1 and 11.3 per million population in different parts of Europe.1
Pregnant women have a 12- to 18-fold increased risk in pregnancy (12/100 000), compared with the non-pregnant population.
Out of all infections withListeria, 16–27 per cent occur in pregnant women.2
The exact cause of its higher prevalence in preg- nancy is not known. Immunosuppression associated with pregnancy results in suppression of cell- mediated immunity in the placenta, due to high con- centration of maternal hormones and other unknown mechanisms.
Approximately 20 per cent of Listeriainfections involve neonatal infection with potentially severe complications, therefore it is important to stop the outbreaks in pregnant woman and the unwanted con- sequences for their unborn fetuses.
Microbiology, Organism and Epidemiology
Out of sevenListeriaspecies, onlyListeria monocyto- genes is an important pathogenic for humans.
Morphologically, they are indistinguishable from diphtheroids, and they are therefore mistaken for contaminants. They can mimic Streptococci, as coc- coid forms are often seen in cultures or smears from infected tissue.
L. monocytogenesis a small, facultative anaerobic, gram-positive,flagellated, linear motile rod, which is non-spore-forming.3It can survive for many months in soil and can be detected in the faeces of animals and humans.
It is mainly acquired by the ingestion of food products, such as meat (hot dogs, deli meat), dairy
products, unwashed raw vegetables, seafood, soft cheeses, unpasteurised milk and dairy products, that have been contaminated.
Outbreaks usually occur due to contaminated food, often commercially produced, as the source of infection.4
Even refrigerated food can be contaminated, prov- ing to be the source in around 11 per cent of cases.5
Many aspects of the epidemiology of listeriosis are unclear because of
• Lack of a sensitive method for strain identification
• Incubation period is very short for gastroenteritis (6 hours to 10 days) but longer for invasive listeriosis (11 to 70 days, with a mean of 28 days)
• Mild or asymptomatic nature of infection
• Variant sources of infection; infecting organism is found in dust, soil, water, sewage, decaying vegetation
• Many species of wild and domestic mammals, avian species, crustaceans, pond trout, ticks and flies harbourListeria
• Milk products (particularly soft cheese) and uncooked vegetables,fish and shellfish, ready-to- eat meat products, ground beef and poultry have all been found to contain the organism
• Up to 70 per cent of the human population harbour the organism in their gastrointestinal tract for short periods (6–16 per cent human faeces) Listeriainfection occurs primarily in elderly peo- ple, in pregnant women and their newborn infants, and in immunocompromised patients including patients with cancer, AIDS, organ transplant recipi- ents or patients on corticosteroid therapy.6
Signs and Symptoms
The majority of people exposed toListeriaare either - asymptomatic or have subclinical infection. Twenty five per cent of culture-positive women report no symptoms. [EL 2]
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• Mildflu-like symptoms, fever.
• Self-limiting febrile gastroenteritis. The fever is usually low-grade or may be significant, ranging from 36.5°C to 40.1°C.
• Watery diarrhoea, nausea, vomiting.
• Headache, backache and pain in joints and muscles.
• Bacteraemia, meningitis and meningoencephalitis occur in 20, 40 and 39 per cent of cases,
respectively.
Signs and symptoms usually lasts for two days followed by complete recovery.
In a series of 191 cases of listeriosis in pregnancy, 32 per cent sufferedflu-like illness and 65 per cent had a fever. Other symptoms included backache (21.5 per cent) (which may be mistaken for a urinary tract infection), headache (10.5 per cent), vomiting/
diarrhoea (7 per cent), muscle pains (4 per cent) and sore throat (4 per cent). Approximately 29 per cent of the women were asymptomatic.6,7[EL 2−]
Invasive infection is rare in healthy populations but tends to affect the immunocompromised, preg- nant or older population.
Diagnosis
8In the Pregnant Woman
• Blood culturesare the standard and only reliable method for diagnosis in cases of fever and symptoms consistent with listeriosis
• Gram stain: the presence of short, gram-positive rods found by Gram stain in maternal blood, urine or faecal matter
• Fetal placentalor cerebrospinalfluid (CSF) specimens support a presumed diagnosis of listeriosis, but the organism is easily confused with Streptococci, diphtheroids and evenHaemophilus
• Stool culture: the American College of Obstetricians and Gynecologists maintains the stool culture has not been validated as a
screening tool and it is not recommended for the diagnosis of listeriosis as it may have low sensitivity8
• Serologic testsare not diagnostically reliable
• Blood culturesare mandatory in case of bacteraemia or sepsis, and CSF culture where meningitis is suspected
• Vaginal and rectal culturesshould also be obtained in symptomatic patients
In Perinatal Listeriosis
Culture can be obtained from
• Blood
• Urine
• Meconium, amnioticfluid, placenta or fetal membranes
• Pus from skin lesions
• Tissue obtained at autopsy
• Cerebrospinalfluid
• Pleuralfluid, respiratory tract and gastric aspirate
• Histopathology and culture of rash
• Culture of other infected tissues (joint, pericardial fluid)
CT scanning or MRI may be useful in detecting abscesses in the brain or liver.
E ff ect of Listeriosis on Pregnancy
During pregnancy, cellular immunity is reduced because of increased progesterone making pregnant women particularly susceptible to intracellular micro- organisms likeL. monocytogenes. Vertical cell-to-cell transmission permits L. monocytogenesto infect the uterus and placenta.
Listeriosis is rarely serious for the pregnant woman herself and symptoms generally resolve after delivery with or without antibiotic therapy. Listeria infection in the pregnant woman rarely causes severe maternal complications such as
• Meningitis
• Adult respiratory distress syndrome
• Endocarditis
Past infection does not offer immunity against reinfection.
Fetal Implications
During pregnancy, fetal infection (90 per cent) can occur via transplacental transmission. Vertical trans- mission can also occur via passage through an infected birth canal or ascending infection after rup- tured amniotic membranes [EL 2]. Once the placenta is infected, it becomes a reservoir for reinfection,6and placental micro-abscesses may be histologically evident.
• First Trimester–miscarriage in 10–20 per cent of cases
• Second Trimester–premature labour in
50 per cent of cases if infection occurs after 20 weeks Section 2: Infections in Pregnancy
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Third Trimester:
• Stillbirth
• Intrauterine death
• Intrauterine growth retardation
• Reduced fetal movements
• Pathological cardiotocography (CTG)
• Non-immune hydrops
• Intracranial calcification
• Chorioamnionitis9
In a retrospective case series study of 222 pregnant women, there were 11 Listeria infections. Nine of those 11 women developed the infection in their third trimester. There were six preterm deliveries (54 per cent) [EL 2]. All six had shown evidence of neonatal Listeriainfections. Two of 11 pregnancies (18 per cent) resulted in fetal death because of spon- taneous abortion and birth of a fetus that died imme- diately after birth.
The above figures indicate the serious neonatal risks ofListeriainfections.
Ultrasound Imaging in Fetal Listeria Infections
10Ultrasound imaging may reveal mild fetal ascites, dilated gall bladder and small bowel loop dilatation, non-immune hydrops, intracranial calcifications, or intrauterine fetal demise.
Fetal surveillance is recommended according to the gestational age.
However, there is no study or data available to suggest the best plan for fetal surveillance and its frequency.
Neonatal Implications
• Listeriosis in the neonate has two different presentations (early or late) depending on the timing of infection.
• Neonatal infection occurs in almost 68 per cent of cases of maternal infection, with complete recovery in approximately 70 per cent
of cases, and long-term sequelae in 12.7 per cent of cases.
• Neonatal death can occur in up to 22 per cent of cases of maternal infection.
1 Early Onset
Early-onset disease occurs within the first seven days of life or soon after birth. The majority of affected infants have poor prognosis due to prema- turity as a result of intrauterine infection (chor- ioamnionitis). Neonatal early-onset listeriosis is non-specific and difficult to distinguish from early- onset group B streptococcal or any other bacterial infection. However, signs of chorioamnionitis with- out rupture of the membranes should raise suspi- cion of Listeria infection and may prompt laboratory diagnosis.11
Clinical features of neonatal infections include:
• Newborns generally pass meconiumin uteroand show fetal compromise on intrapartum fetal heart rate (FHR) tracings.
• Respiratory distress or pneumonia in 38 per cent, with rapid breathing, and grunting which may include cyanotic episodes.
• Poor feeding and fever are common presenting symptoms.
• Septicaemia and meningitis are the most common clinical manifestation.
• Severe infection causes skin lesions (slightly elevated, 1 to 2 mm pale patches on a bright erythematous base) mostly seen on the infant’s back and lumbar area called granulomatosis infantisepticum.
• Disseminated granuloma abscesses involve the liver, spleen, adrenal glands, lungs, oesophagus, the posterior pharyngeal wall and placenta.
• Neutropenia is more characteristic of severe infection. Thrombocytopenia sometimes occurs and anaemia is common, most likely secondary to the haemolysin listeriolysin.
On chest X-ray, non-specific pneumonia is common.
2 Late Onset
Late-onset neonatal infection occurs from one to eight weeks of life and typically affects full-term infants whose mothers had uncomplicated pregnancies.
The infants are usually healthy at birth and symptoms manifest at a mean of 14 days of life, strongly suggesting acquired horizontal postpar- tum infection at delivery from the maternal genital tract or through nosocomial infection (delivery rooms or nurseries).
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