Healthcare-Associated Bacterial Infections of the Central Nervous System, Upper and Lower Respiratory Tracts, and Skin in Pediatric Patients



Healthcare-Associated Bacterial Infections of the Central Nervous System, Upper and Lower Respiratory Tracts, and Skin in Pediatric Patients


W. Matthew Linam

Terry Yamauchi



Clinicians involved in the care of children must be alert for signs or symptoms of healthcare-associated infections in their pediatric patients. Infections involving the central nervous system, respiratory tract, and skin can occur even under optimal conditions. Clinicians must be aware of the potential infecting microorganisms and should understand the pathogenesis of these illnesses. An understanding of these factors allows for appropriate therapy and infectioncontrol measures.


CENTRAL NERVOUS SYSTEM INFECTIONS

Healthcare-associated infections of the central nervous system include intracranial infections, meningitis or ventriculitis, and shunt infections. Central nervous system infections account for 2% to 17% of all healthcare-associated infections in infants in intensive care units (1,2,3,4,5,6,7). Most of these infections involve surgical procedures and/or manipulation/trauma within the central nervous system. Information concerning pediatric intensive care units is less readily available; although some investigators have demonstrated a central nervous system infection rate of 25% in their pediatric intensive care units, others have had no occurrences (8,9).


Intracranial Infections

Pathogenesis Intracranial infections, such as brain abscesses, are not commonly encountered and should meet the criteria from the Centers for Disease Control and Prevention (CDC) in Table 49-1 for diagnosis (10). Brain abscesses commonly form via direct spread from a contiguous source or via hematogenous spread from a distant source. In approximately one-third of situations, however, no predisposing factors are identified. Respiratory diseases such as chronic sinusitis, otitis media, and mastoiditis account for the majority of sites from which microorganisms can extend directly into the brain (11,12). Patients who develop abscesses resulting from contiguous spread usually have a single abscess in the proximity of the infected region. Abscesses acquired through the hematogenous route tend to follow the course of the middle cerebral artery and cause abscesses in the frontal and parietal regions. Cyanotic congenital heart disease with right-to-left shunts or pulmonary arteriovenous fistulas predisposes patients to brain abscess formation (13,14). The most common lesion encountered in such patients is tetralogy of Fallot (15). A healthcare-associated brain abscess is particularly likely in patients who have suffered head trauma or who have undergone neurosurgical procedures. Approximately 6% to 11% of abscesses are in patients with head trauma or neurosurgical procedures, and their symptoms usually develop within 10 days to 2 months following the inciting episode (13,14,16,17).

Etiology Brain abscesses are often polymicrobial in origin, but when they occur in patients who have had head injuries or neurosurgical procedures, Staphylococcus aureus—including methicillin-resistant S. aureus (MRSA)— followed by the viridans streptococci and Streptococcus pneumoniae are the most common microorganisms isolated (13, 14, 15, 16 and 17). Abscesses in patients with complex congenital heart disease include anaerobes, viridans streptococci, microaerophilic streptococci, enterococci, and Haemophilus species. The etiologic agents in patients with a history of chronic sinusitis or otitis media are anaerobes, gramnegative rods (Proteus, Pseudomonas, Haemophilus), and S. aureus.

Clinical Manifestations Symptoms associated with a brain abscess include fever (68%), headache (66%), vomiting (59%), focal neurologic deficits (46%), seizures (44%), papilledema (39%), and meningeal signs (36%) (18). Papilledema and meningeal signs may not be present in patients younger than 2 years (13,14). The classic triad of symptoms—headache, fever, and focal neurologic deficits—is demonstrated in <30% of patients (14).









TABLE 49-1 Definitions for Central Nervous System Infections in Pediatric Patients













Intracranial Infection




  • Microorganism must be cultured from the brain tissue or dura



  • Patient shows evidence of infection at surgery or by histopathologic examination



  • Patient indicates two or more of the following without another recognizable cause: headache, dizziness, fever (>38°C), localizing neurologic signs, change in mental status; these symptoms must be followed by institution of appropriate antimicrobial therapy with the microorganism seen on microscopic examination, or there must be a positive antigen test, radiographic evidence of infection, or a diagnostic antibody test



  • Criteria are similar for patients younger than 12 mo with the inclusion of hypothermia (<37°C), apnea, or bradycardia


Meningitis/Ventriculitis




  • Microorganism is isolated from the cerebrospinal fluid



  • Appropriate antimicrobial therapy is instituted, and the patient has one or more of the following: fever (>38°C), headache, stiff neck, meningeal signs, cranial nerve signs, irritability; and one of the following laboratory abnormalities: increased white cells, elevated protein, and/or decreased glucose in the cerebrospinal fluid; positive gram stain; positive blood culture; positive antigen detection; or a diagnostic antibody test



  • Criteria are similar for patients <12 mo with the inclusion of hypothermia (<37°C), apnea, and bradycardia


(Adapted from Horan TC, Andrus M, Dudeck MA. CDC/NHSN surveillance definition of healthcare-associated infection and criteria for specific types of infections in the acute care setting. Am J Infect Control 2008;36:309-332.)


Diagnosis The diagnosis of a brain abscess can be established by cerebral imaging using cranial ultrasonography, computed tomography, or magnetic resonance imaging.

Prevention Prophylactic antimicrobial agents may prevent the development of brain abscesses in certain situations. Antimicrobial prophylaxis to prevent infective endocarditis is currently only recommended for patients with cardiac conditions that place them at the highest risk for complications from infective endocarditis (Table 49-2) (19,20). Antimicrobial prophylaxis is indicated in patients before dental procedures that involve the manipulation of the periapical region of the teeth or the gingival mucosa or the perforation of the oral mucosa. Prophylaxis should also be considered for invasive respiratory procedures that involve incision or biopsy of the respiratory mucosa and infected skin, skin structure, or musculoskeletal tissue (19). Recommended prophylaxis regimens are outlined in Table 49-3.

Antimicrobial prophylaxis for neurosurgical procedures has been demonstrated to be effective for clean and clean-contaminated procedures (21, 22, 23, 24, 25 and 26). Antibiotics should be started within 60 minutes of the skin incision with the exception of vancomycin and fluoroquinolones, which should be started 60 to 120 minutes before the skin incision. For procedures lasting longer than 4 hours, antibiotic redosing should be based on the half-life of the antibiotic, but antibiotics should be discontinued within 24 hours after surgery (27). Multiple regimens have been used involving vancomycin (21), vancomycin/gentamicin (24), cefazolin/gentamicin (26), piperacillin (22), cloxacillin (25), and cefuroxime (28). Despite the multiple combinations that have been used, all the regimens should include activity against staphylococci. It is recommended that patients undergoing clean or clean-contaminated neurosurgical procedures receive antimicrobial prophylaxis with cefazolin or vancomycin as the drugs of choice (23,29). Patients known to be colonized with MRSA should receive vancomycin for prophylaxis (27). In hospitals with high rates of healthcare-associated gram-negative infections, consideration should be given to including antimicrobial agents in the regimen that are active against the prominent gram-negative microorganisms as well.








TABLE 49-2 Cardiac Conditions Associated with the Highest Risk of Adverse Outcome from Endocarditis for which Prophylaxis with Dental Procedures is Reasonable

















Prosthetic cardiac valve or prosthetic material used for cardiac valve repair


Previous IE


Congenital heart disease (CHD)a




  • Unrepaired cyanotic CHD, including palliative shunts and conduits



  • Completely repaired congenital heart defect with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first 6 mo after the procedureb



  • Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (which inhibit endothelialization)


Cardiac transplantation recipients who develop cardiac valvulopathy


a Except for the conditions listed above, antibiotic prophylaxis is no longer recommended for any other form of CHD.

b Prophylaxis is reasonable because endothelialization of prosthetic material occurs within 6 mo after the procedure.


(Reprinted with permission from Wilson W, Taubert KA, Gewitz M, et al. Prevention of infective endocarditis: guidelines from the American Heart Association. Circulation 2007;116:1736-1754 ©2007, American Heart Association, Inc.)










TABLE 49-3 Regimens for a Dental Procedure








































































Regimen: Single Dose 30-60 min before Procedure


Situation


Agent


Adults


Children


Oral


Amoxicillin


2 g


50 mg/kg


Unable to take oral medication


Ampicillin


2 g IM or IV


50 mg/kg IM or IV



OR



Cefazolin or ceftriaxone


1 g IM or IV


50 mg/kg IM or IV


Allergic to penicillins or ampicillin—oral


Cephalexina,b


2 g


50 mg/kg



OR



Clindamycin


600 mg


20 mg/kg



OR



Azithromycin or clarithromycin


500 mg


15 mg/kg


Allergic to penicillins or ampicillin and unable to take oral medication


Cefazolin or ceftriaxoneb


1 g IM or IV


50 mg/kg IM or IV



OR



Clindamycin


600 mg/kg IM or IV


20 mg/kg IM or IV


a Or other first- or second-generation oral cephalosporin in equivalent adult or pediatric dosage.

b Cephalosporins should not be used in an individual with a history of anaphylaxis, angioedema, or urticaria with penicillins or ampicillin.


IM, intramuscular; IV, intravenous.


(Reprinted with permission from Wilson W, Taubert KA, Gewitz M, et al. Prevention of infective endocarditis: guidelines from the American Heart Association. Circulation 2007;116:1736-1754 ©2007, American Heart Association, Inc.)



Meningitis and Ventriculitis

Pathogenesis Meningitis or ventriculitis is usually the result of a bacteremia. The bacteria gain access to the central nervous system from the blood in the region of the choroid plexus. Meningitis less commonly develops as a complication of endocarditis, pneumonia, or thrombophlebitis. There may also be a direct extension from a chronic respiratory source (i.e., mastoiditis) or as a complication of trauma (i.e., basilar skull fracture), an anatomic defect of the cribriform plate, or a direct communication between the skin and meninges (meningomyelocele) (30). Some degree of ventriculitis can be demonstrated in most cases of bacterial meningitis, but ventriculitis is more common as an infectious complication of ventricular shunting. The predominant microorganisms involved in healthcare-associated meningitis or ventriculitis are different from those involved in community-acquired disease. Contributing factors include the age, immune status, and antibiotic history of the patient. The diagnostic criteria for healthcare-associated meningitis or ventriculitis are outlined in Table 49-1.

Etiology In children older than 3 months, the common pathogens causing meningitis have traditionally included Haemophilus influenzae type B, S. pneumoniae, and Neisseria meningitidis. Because of the efficiency of the Haemophilus vaccines, however, this microorganism is no longer the predominant pathogen (31). For children younger than 3 months, group B β-hemolytic streptococci (GBS), Escherichia coli, and Listeria monocytogenes are the most frequent causes of meningitis (32). Newborns become colonized with these microorganisms from passage through the birth canal and may develop illness within hours after birth. If illness occurs within the first 6 days of life, it is considered an early-onset illness. Infections that develop after 6 days of life are considered late-onset illnesses. Early-onset illnesses are due to microorganisms harbored in the mother’s birth canal. Microorganisms that cause late-onset disease may have been transmitted from the mother or may have been acquired from caregivers or the environment.

Most healthcare-associated cases of meningitis in children older than 3 months are due to the staphylococci, although enterococcal and gram-negative enteric (E. coli, Klebsiella, Enterobacter, Proteus) infections do occur (2,33). When staphylococcal meningitis occurs, there is an associated defect in the central nervous system resulting from surgery or trauma in approximately 75% of cases (34,35). Therefore, most cases are due to direct extension of the microorganism instead of hematogenous spread. Spread of the more traditional microorganisms such as N. meningitidis and H. influenzae occurs via the respiratory route, and therefore, respiratory spread is a potential hazard for healthcare-associated transmission. These microorganisms are responsible for secondary diseases in family members but only rarely have been associated with healthcare-associated infections of the central nervous system (36).

Early-onset GBS disease usually manifests itself as respiratory distress with bacteremia. Most early-onset disease, regardless of the microorganism, usually lacks meningeal involvement. Meningeal involvement is a common manifestation in late-onset disease (37) (see Chapter 32). Most
newborns who develop meningitis while hospitalized are in neonatal intensive care units. Therefore, clinicians should be concerned about the bacteria that are known to be present in each nursery. Outbreaks of meningitis in neonatal intensive care units have been attributed to several microorganisms, both gram-positive and gram-negative, including S. aureus, Staphylococcus epidermidis, Serratia, Klebsiella, and Citrobacter (7,38, 39 and 40) (see Chapter 52).

Clinical Manifestations Children with meningitis usually have signs and symptoms relating to their central nervous system, whereas infants may not. The diagnosis of meningitis must be considered in any patient with fever, altered mental status, and meningismus.

Diagnosis A lumbar puncture is the method of choice for establishing this diagnosis. An increased number of white blood cells with a polymorphonuclear predominance, elevated cerebrospinal fluid (CSF) protein levels, and decreased glucose levels are typically found with bacterial meningitis. The CSF should be sent for gram staining, and CSF and blood should be cultured for bacteria to aid in finding the etiologic agent. Bacterial antigens are less helpful because the more common healthcare-associated pathogens are not included in such panels. Recently, polymerase chain reaction (PCR) has become more readily available for the detection of bacterial meningitis. Broad-range PCRs targeting the 16S rRNA gene and specific PCRs for the detection of pathogens such as S. pneumoniae and Neisseria meningitides can assist in diagnosing bacterial meningitis, particularly in situations in which the patient has received antibiotics prior to the collection of spinal fluid (41, 42, 43 and 44).

Prevention To aid in the prevention of healthcare-associated disease, patients admitted to the hospital with meningitis resulting from N. meningitidis or S. pneumoniae should be placed on Droplet Precautions for the first 24 hours of hospitalization, and all contacts of the patient should observe strict hand washing (45). Antibiotic prophylaxis may be indicated for household or day-care contacts who have had direct exposure to the oral secretions of patients who have an N. meningitidis infection. Only hospital personnel with exposure to a patient’s respiratory secretions through situations such as unprotected mouthto-mouth resuscitation, intubation, or airway suctioning should receive prophylaxis (see Chapter 76). Rifampin, 10 mg/kg (maximum of 600 mg), every 12 hours for 2 days is indicated for persons aged 1 month or older. Contacts who are younger than 1 month should receive 5 mg/kg every 12 hours for 2 days. Affected individuals should be alerted to the potential side effects of the medication: urine and other secretions are discolored (orange or red), contact lenses can become permanently discolored, and rifampin may alter the activity of birth control pills.

Pregnant women should be excluded from rifampin prophylaxis (46). Options for individuals unable to take rifampin include ceftriaxone or ciprofloxacin (47). Ceftriaxone given in a single intramuscular injection at a dose of 125 mg for children younger than 15 years and 250 mg for others has been demonstrated to effectively eradicate the meningococcal carrier state with group A N. meningitidis (48). A single oral dose of ciprofloxacin, 20 mg/kg (maximum dose 500 mg), has been demonstrated to be effective in adults but cannot be used in children or in pregnant or lactating women (49). Ceftriaxone should be used in pregnant women. These options should only be considered in circumstances in which rifampin cannot be used.

Meningococcal vaccine can be used as an adjunct to chemoprophylaxis in outbreaks caused by serogroups that are included in the vaccine (A, C, Y, and W-135). For adults and children older than 2 years, the preferred vaccine is the tetravalent meningococcal (A, C, Y, and W-135) conjugate vaccine, but the tetravalent meningococcal (A, C, Y, and W-135) polysaccharide vaccine may also be used. Serogroup B is not contained in the vaccine. The tetravalent meningococcal (A, C, Y, and W-135) polysaccharide vaccine has been used in children younger than 18 months. This is given as 2 doses 3 months apart to control outbreaks (50).

For trauma patients with basilar skull fractures, antimicrobial prophylaxis for the prevention of meningitis is controversial (51). Currently, antimicrobial prophylaxis does not appear to decrease the incidence of meningitis after a basilar skull fracture (51). Surgical intervention should be performed when there is no evidence of healing and/or repeated infection occurs. For open skull fractures, antibiotic prophylaxis is generally recommended (52).

The prevention of early-onset meningitis in neonates begins with good prenatal care and intervention strategies to prevent the transmission of potentially harmful microorganisms to the newborn infant (53). To prevent early-onset neonatal GBS disease, all pregnant women should have vaginal and rectal cultures for GBS at 35 to 37 weeks of gestation. Women identified as carriers during the current pregnancy should receive intrapartum antibiotic prophylaxis at the onset of labor or rupture of membranes. Intrapartum prophylaxis should be administered to all women who have had a previous infant with invasive GBS disease or who are found to have GBS bacteriuria during the current pregnancy. If the results of the GBS screen are not known at the onset of labor or rupture of membranes, intrapartum antimicrobial prophylaxis should be administered if any of the following risk factors are present: gestation of <37 weeks, prolonged rupture of membranes ≥18 hours, or intrapartum temperature ≥38°C. The antimicrobial agent of choice is penicillin G (5 million U initially and then 2.5 million U every 4 hours) given intravenously until delivery. Intravenous ampicillin (2 g initially, followed by 1 g every 4 hours until delivery) can be used, but penicillin is preferred because of its narrow spectrum. Intravenous cefazolin or vancomycin can be used for penicillin-allergic patients. Because of the increasing prevalence of resistance, clindamycin and erythromycin should not be used for antibiotic prophylaxis for GBS. The management of infants born to mothers who have received chemoprophylaxis should be based on the gestational age of the infant, the number of doses of the prophylactic agent received, and the clinical findings of the infant (54).


Shunt Infections

Pathogenesis Approximately 4.5% to 25% of patients who have undergone CSF shunting procedures develop infectious complications (55, 56, 57, 58 and 59). Risk factors for infection include young age of the patient (<3 months), inexperienced surgeons, prolonged shunting procedures,
and distal catheter tip location (60, 61, 62 and 63). Shunt infections usually occur within 2 months after placement; most of these infections are caused by transient or permanent bacterial inhabitants of the skin. The latter observations suggest that direct inoculation in the perioperative period is probably the pathogenesis of this infection (64).

Etiology Staphylococci are responsible for approximately 75% of infections; S. epidermidis is the primary agent in 50% and S. aureus in 25% (55,56,58). Infections with gram-negative enteric microorganisms (E. coli, Klebsiella, Proteus) and Pseudomonas account for approximately 20%; the remainder of infections are caused by less-common microorganisms such as Enterococcus, viridans streptococci, N. meningitidis, micrococcus, H. influenzae, diphtheroids, Propionibacterium, and Corynebacterium (56,58,65, 66, 67 and 68).

Clinical Manifestations The most common symptoms of shunt infections are usually symptoms of shunt malfunction. Headache, irritability, lethargy, nausea, and change of mental status are common. Although fever is usually present, approximately 10% to 20% of children are afebrile (56,58). In most shunt infections, signs of meningeal irritation are absent because there is no communication between the infected ventricle and the CSF.

Diagnosis Shunt infections should be suspected in any patient who has a ventricular shunt with complaints of malfunction. Fluid from the shunt or ventricle is needed to secure the diagnosis, and the fluid usually displays an increase in the white blood cell count (>10 cells/mm3). CSF should be cultured aerobically and anaerobically and also plated on media for the isolation of fungi. Extreme care should be used when obtaining a CSF specimen from a ventricular shunt bubble. Neurosurgical consultation should be considered before attempting to violate the shunt. The area should be cleaned before penetration with a needle to avoid contaminating the shunt. If patients have concomitant complaints of abdominal distention, peritonitis, shunt wound infection, erythema, or swelling along the shunt tract or if they appear toxic, the shunt should be assumed to be infected.

Prevention The role of prophylactic antimicrobial agents for the prevention of shunt infections has been controversial with the protective efficacy demonstrated to vary widely (5-84%) (23). A meta-analysis performed by Langley et al. (69) showed that antibiotic prophylaxis resulted in a 50% reduction in postoperative infections after cerebrospinal shunt insertion. In a recent systematic review, perioperative antibiotic prophylaxis was associated with a significant reduction in shunt infections (70). Based on current data, the use of antibiotic prophylaxis with an antistaphylococcal agent (i.e., nafcillin, cefazolin, vancomycin) beginning before the procedure and continuing for up to 24 hours after the procedure is recommended (70). Recently, silicone catheters impregnated with rifampin and clindamycin have been developed to help reduce the incidence of shunt infections. Initial experience reveals that antibiotic-impregnated catheters appear to be well tolerated and can reduce the incidence of shunt infection in children and adults (71, 72 and 73).

Occasionally, patients require external ventricular drains. These drains may be placed for limited periods after surgery or trauma or when the release of ventricular fluid is required to combat increased intracranial pressure. Catheters are placed directly into the ventricle and drain into an external receptacle. Patients who require these drains are at an increased risk for infectious complications; therefore, CSF specimens should be carefully extracted when these devices are entered. Regular catheter exchange does not prevent infections associated with external ventricular drains (74).


RESPIRATORY TRACT INFECTIONS


Upper Respiratory Tract Infections

Most healthcare-associated upper respiratory tract infections are nonbacterial and appear approximately 2 weeks after admission (2,6). Respiratory syncytial virus, adenovirus, and influenza virus account for most of these infections (75) (see Chapter 48). The role of bacteria in healthcare-associated upper respiratory tract infections is manifested predominantly in sinusitis and otitis media. Less commonly encountered problems include pharyngitis, bacterial tracheitis, and diphtheria.

Pharyngitis Group A Streptococcus is a common cause of community-acquired pharyngitis but not of healthcareassociated disease. Patients are rarely admitted to the hospital for a streptococcal throat infection but may be admitted for complications of this infection, such as a peritonsillar or retropharyngeal abscesses. When such complications occur, cultures often reveal multiple microorganisms including S. aureus, gram-negative microorganisms, and anaerobic microorganisms (76,77). Secondary cases of disease resulting from Streptococcus pyogenes are higher among siblings than among adult contacts. Rates of infection may be as high as 50% for sibling contacts compared with 20% for adult contacts. Asymptomatic, culture-positive individuals (children and adults) are well documented and may be the source for some infections (78). The most important means of controlling group A streptococcal infections, therefore, is early identification and treatment of the disease. Although many contacts develop illness, asymptomatic contacts should not be cultured or treated. Symptomatic contacts should undergo a throat culture and be treated if group A Streptococcus is isolated (78).

Bacterial Tracheitis Bacterial tracheitis is a bacterial infection thought to be secondary to a primary viral respiratory infection, usually parainfluenza or influenza viruses (79,80). The viral infection may cause local mucosal damage, alter the patient’s immune response, or both, thus leading to a secondary bacterial infection (81,82). The most common microorganism involved is S. aureus. Other implicated microorganisms include S. pneumoniae, H. influenza, and S. pyogenes (79,80). Before the availability of H. influenzae conjugate vaccines, this disorder was as common as epiglottitis, but because of a dramatic decrease in the incidence of invasive H. influenzae disease, bacterial tracheitis may now be more common (79). The patient with
bacterial tracheitis usually has a waning viral respiratory illness when the fever rises and stridor begins or worsens. Patients assume any position that maximizes their airflow, not just the sniffing position as demonstrated with epiglottitis. Patients can deteriorate quickly and frequently require intubation to maintain patency of the airway and facilitate frequent suctioning. Endoscopic examination, which should be performed in an operating room, reveals copious, tenacious, purulent secretions above the subcricoid trachea. No isolation is required. Early recognition and treatment is the only method to prevent life-threatening illness.

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Jun 22, 2016 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on Healthcare-Associated Bacterial Infections of the Central Nervous System, Upper and Lower Respiratory Tracts, and Skin in Pediatric Patients

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