History and exam
Key diagnostic factors
common
presence of risk factors
In neonates, the key risk factors include onset in first week of life, premature rupture of membranes, preterm delivery, maternal fever during labour, chorioamnionitis, siblings of babies who have had GBS infection, maternal age <20 years, and heavy maternal colonisation (bacteriuria). For late-onset infection, obstetric complications are absent.[6][12][22][23][35]
In infants and children, key risk factors include renal disease, neurological disease, malignancy, and immunosuppression.[7]
In adults, the key risk factors include age >60 years, black ethnicity, residency in a nursing home, pregnancy, urinary tract infection, diabetes, obesity, immunosuppression, renal/ liver disease, placement of central venous catheter, underlying malignancy, neurological disease, and the presence of a central line or break in skin integrity (e.g., diabetic foot ulcers, pressure sore).[7][6][20][21][37]
fever
Fever is a common presenting symptom as with any other bacterial infection, but it is often absent in neonates and older people.
Neonates often present with temperature instability rather than fever.
symptoms of meningitis
Include headache, photophobia, or neck pain or stiffness.
May be caused by meningeal inflammation and can indicate meningitis.
Symptoms of meningeal inflammation are often absent in children <2 years of age.
signs of meningitis
Seizures can develop as a result of meningitis, especially in neonates.
Bulging fontanelles indicate raised intracranial pressure and meningitis in neonates.
Positive Kernig's sign indicates meningeal inflammation and suggests meningitis. Elicited by having the patient lie supine and flexing the thigh so that it is at a right angle to the trunk, and extending the leg at the knee joint. Inability to extend the leg completely due to pain is considered positive.
Positive Brudzinski's sign also indicates meningeal inflammation and suggests meningitis. Due to inflammation of lumbosacral nerve roots. When the neck is abruptly flexed passively, meningeal irritation causes involuntary flexion of the hips and knees.
Signs of meningeal inflammation are often absent in children <2 years of age.
symptoms of sepsis
Confusion.
signs of sepsis
Hypotension, tachycardia, poor capillary perfusion, or tachypnoea.
Intravascular pressures are decreased by vasodilation and dehydration.
symptoms of pneumonia
Productive cough, dyspnoea, tachypnoea, pleuritic chest pain, or increased work of breathing.
signs of pneumonia
Cyanosis, nasal flaring, intercostal or subcostal indrawing, decreased breath sounds, auscultatory crackles, and pleural rub.
symptoms of urinary tract infection
Dysuria, frequency, urgency, haematuria, or back/flank pain.
signs of urinary tract infection
Suprapubic tenderness or costovertebral angle tenderness.
symptoms of cellulitis
Skin erythema, warmth, discomfort, tenderness, or oedema.
signs of cellulitis
Raised erythema with clearly demarcated margins or macular erythema with indistinct borders.
symptoms of septic arthritis
Joint erythema, swelling, or pain, or decreased range of motion in joint.
signs of septic arthritis
Hot, swollen, tender joint with joint effusion.
symptoms of conjunctivitis
Watery, mucoid, or purulent ocular discharge, ocular tenderness, or eyelids stuck together in morning.
symptoms of sinusitis
Nasal discharge or facial pain.
signs of sinusitis
Nasal mucosal erythema.
symptoms of otitis media
Otalgia.
signs of otitis media
Bulging tympanic membrane or myringitis.
symptoms of endometritis
Lower abdominal pain.
signs of endometritis
Uterine tenderness.
signs of chorioamnionitis
Abnormal amniotic fluid, fetal tachycardia or decreased heart rate variability, or uterine tenderness.
Amniotic fluid may be foul-smelling or grossly purulent.
Other diagnostic factors
common
non-specific signs of infection in neonate
Lethargy, irritability, poor appetite/feeding, grunting, pallor, hypotonia, increased respiratory rate, respiratory distress.
non-specific signs of infection in older patients
Hypothermia or confusion.
symptoms of intra-abdominal infection
Abdominal pain, decreased bowel movements, or nausea or vomiting.
signs of intra-abdominal infection
Tender rigid abdomen, guarding, rebound abdominal tenderness, or decreased or absent bowel sounds.
mid-gestation abortion or pre-term labour
May occur in pregnant women with GBS infection.
Risk factors
strong
0 to 7 days of age
80% of childhood GBS infections occur in the first 7 days of life, after exposure to the bacteria during labour or before delivery, including aspiration of contaminated amniotic fluid.[22]
maternal fever during labour
Defined as temperature ≥38°C (100.4°F).
In neonates with early-onset GBS disease, maternal intrapartum fever has been found in 18% to 48% of cases.[12][23]
Maternal fever was also found in one third of term neonates asymptomatic at birth but who subsequently developed early-onset sepsis.[24]
One study found that the risk of early-onset GBS disease rose significantly if maternal fever exceeded 38.3°C (101°F), with a fever of 39°C (102.5°F) being associated with 4 times the risk of a fever of 38.3°C (101°F).[25]
premature rupture of membranes (PROM)
Predisposes to ascending uterine infection, and is an independent risk factor for early-onset disease in the neonate.[6][26]
Risk of infection increases with the duration of rupture before delivery.
PROM >18 hours was present in 13.8% of cases of early-onset GBS disease in one study, and in 53% of mothers with PROM >12 hours in a separate study.[12][23]
previous baby with GBS disease
maternal GBS colonisation
Well-recognised risk factor for early-onset GBS infection.
Approximately 1% to 2% of babies born to colonised mothers will develop early-onset GBS infection.[6]
Risk of disease is related to the degree of colonisation of the infant, which is directly related to the heaviness of colonisation in the mother.[6]
GBS bacteriuria during pregnancy
Marker of heavy colonisation, and therefore of increased risk of perinatal transmission and GBS disease in the neonate.[6]
preterm delivery (<37 weeks)
low birth weight (<2500 g)
deficient maternal-specific IgG at term
Maternal-specific IgG protects term infants from GBS disease. The IgG must be specific to the capsular serotype being carried at the time of delivery.[16][17][27]
Risk is directly related to the level of antibody carried. For example, there is a 75% decreased risk for delivering a neonate with early-onset disease after 34 weeks' gestation if maternal-specific IgG level is ≥2 micrograms/mL, and a 91% decreased risk if level is ≥10 micrograms/mL.[16]
twin sibling with GBS disease
Risk is probably multifactorial, including risk of exposure, colonisation status of mother, obstetric complications, prematurity, and presence of maternal-specific antibody.[32]
Exact risk is not known, but 50% of siblings in one small study developed the disease.[33]
In one case report, late-onset infection resulted in fatal meningitis in one twin, whereas the other twin made a full recovery. GBS isolates were identical. Clinical variables included longer duration of fever prior to antibiotic treatment and the development of neutropenia.[32]
Sibling should be monitored closely for evidence of disease. Some recommend investigation followed by empirical treatment of a twin sibling regardless of whether symptoms are present.[33][34]
maternal age <20 years
chorioamnionitis
Risk factor for early-onset neonatal infection due to increased risk of exposure to GBS.[6]
Aspiration of amniotic fluid can result in respiratory tract infection.
GBS may not be the sole causative pathogen, as other potentially pathogenic organisms may also colonise the vagina.
age >60 years
Risk of invasive disease increases with age, with 57% of cases of invasive disease in non-pregnant adults occurring in those >60 years of age.[20]
More than half of deaths from GBS disease are in patients aged >60 years, despite colonisation rates similar to those in women of childbearing age.[37]
The exact reason for the increased risk of infection with increasing age is incompletely understood, but may be due to waning cell-mediated immunity. Non-specific symptoms in older people and a blunted febrile response may contribute to increased mortality through diagnostic delay.[37]
Most invasive infections in older people are associated with other comorbidities likely to contribute to the increased mortality.[38]
pregnancy
Well-recognised risk factor for GBS disease.
Approximately 10% to 30% of pregnant women are colonised with GBS in the rectum or vagina.[6]
multiparity
diabetes
Well-recognised risk factor for invasive GBS disease in all populations.[13][37][41]
Reasons for increased incidence include a blunted immune response with impaired phagocytosis, and the presence of other factors that provide a portal of entry for GBS such as peripheral vascular disease, foot ulcers and breaks in skin integrity, an increased risk of urinary tract infection, and an increased risk of admission to hospital and instrumentation.[26]
obesity
advanced hepatic disease
renal disease
Increased risk of disease in this population is probably related to immunosuppression, presence of indwelling devices (e.g., central venous catheters, peritoneal dialysis catheter), frequent need for hospital admission, and presence of other risk factors (e.g., diabetes, peripheral vascular disease).
About 13% of cases of invasive disease in children aged 1 to 14 years were associated with renal disease in one study.[7]
Approximately 14% to 21% of cases of invasive disease in non-pregnant adults are associated with renal disease.[20][45][46]
presence of central venous catheter
Provides portal of entry for GBS.
Strongly associated with nosocomial infection.[21]
urological disorders
Provides portal of entry for GBS, which is a recognised cause of urinary tract infection (UTI).
Urological disorders predispose patients to UTIs and are present in 13% to 22% of cases of invasive disease in non-pregnant adults.[20][21]
Neurogenic bladder has been identified as a risk factor for community-acquired disease.[21]
break in skin integrity or skin ulcers
Examples include diabetic foot ulcer and pressure sore.[47]
Provides portal of entry for GBS and is often associated with other underlying condition that predisposes to GBS disease (e.g., diabetes).
Decubitus ulcer has been identified as a risk factor in a population-based study of invasive disease in non-pregnant adults.[21]
neurological disease
Associated with invasive disease in children aged 1 to 14 years.[7]
Also associated with disease in non-pregnant adults. Aspiration or suspected aspiration and subsequent pneumonia is common in this group.[21]
Exact reason for the association has not been studied, but is likely to be multifactorial, including risk of aspiration, exposure to healthcare facilities, and the presence of indwelling devices.
immunosuppression
Associated with invasive disease in children and adults.[7][48]
In one analysis of surveillance data, 23% of children aged 1 to 14 years with invasive GBS disease had an underlying immunosuppressive condition (not further defined).[7]
In non-pregnant adults, neutropenia and glucocorticoid use may increase the risk of GBS infection.[48]
nursing-home resident
Incidence of disease higher in nursing-home residents than in older community residents of the same age.[37][49]
The reason for increased incidence is not known, but it is likely related to increased burden of predisposing conditions and reduced physical reserves in nursing-home residents, possibly coupled with transmission within the nursing home.[37][49]
black or Hispanic race
In both adult and early-onset neonatal GBS disease, the incidence in black people is approximately double that in white people.[20][23][29]
Most studies in the US show an increased incidence of disease in black people in all age groups, with an incidence of invasive disease of 12.8 per 100,000 population compared with 6.5 per 100,000 population among white people and 5.1 per 100,000 population for other races combined.[7]
The exact reason for the increased incidence is not known, but may at least partly reflect socioeconomic status.
One UK cross-sectional study found GBS colonisation rates during pregnancy were significantly higher in black women than in white or South Asian women, at 39.5%, 27.4%, and 23.3%, respectively.[39]
Increased risk of early-onset neonatal disease in Hispanic infants (similar to the risk in black infants) has also been documented.[29]
malignancy
Associated with GBS disease in non-pregnant adults and children.[7]
Type of malignancy varies from study to study, with the variation presumably related to the case mix.
Relative risk associated with malignancy declines with age as the incidence in the comparator population increases.[20]
In one study, breast cancer was associated with GBS disease but not malignant disorders in general.[21]
Another study found that patients with breast cancer were at greater risk of recurrent GBS infection, but they experienced lower rates of severe GBS disease than patients with other cancer types, including lymphoma.[50]
Exact reason for the association has not been studied, but is likely to be multifactorial, including risk of aspiration, exposure to healthcare facilities, and the presence of indwelling devices.
weak
obstetric manipulation
Associated with early-onset disease.
Theoretically, obstetric intervention can facilitate ascending infection if mother is colonised, and some cases support such a mechanism (e.g., GBS scalp monitor abscess).[20] However, there have been no randomised controlled trials to compare intervention with no intervention, and evidence supporting such an association is weak.
Risk associated with manipulation is difficult to separate from risk associated with prolonged and/or complicated delivery, but there is a theoretical risk that no intervention may prolong labour and therefore increase the risk of infection.
presence of urinary catheter
Provides portal of entry for GBS.
Present in 15.7% of cases of invasive disease in non-pregnant adults, but a significant association was not demonstrated on multivariate analysis.[45]
HIV infection
Identified as a risk factor for disease in some studies, but not others, which probably reflects the differences in the case mix of the populations studied.[20][45]
The introduction of highly active antiretroviral therapy is likely to have reduced the risk of disease associated with HIV.
There appears to be no significant difference between GBS colonisation rates in HIV-infected and uninfected pregnant women, although this could be due to antibiotic prophylaxis in HIV-infected pregnant women.[51][52][53]
Infants exposed to, but uninfected by, HIV may be more likely to develop late-onset GBS disease. Possible mechanisms include disruption of the neonatal gut microbiome and a reduced tendency of HIV-infected women to breastfeed.[52][53]
trauma
Provides portal of entry for GBS.
Was strongly associated with disease in a population-based study of invasive disease in non-pregnant adults in South Africa: 25% of patients had a history of trauma, 60% of them involving penetrating injuries; 60% of the trauma-associated cases were acquired in hospital.[54] The mean age of the patients in this study (i.e., 45.6 years) was lower than for most other studies, and association of disease with trauma may reflect a difference in epidemiology of disease in developing countries.
asthma
consumption of placenta capsules
Late onset infant GBS infection has been associated with consumption of capsules containing dehydrated placenta by the mother.[55]
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