Professional Documents
Culture Documents
98372
98372
BY
Yasser A. Elbayoumi
Supervisor
September 2011
Abstract
Epidemiology of septicemia at neonatal intensive care units in Gaza city hospitals
Background: The prevalence of healthcare-associated neonatal bloodstream
infections is increasing and results in significant morbidity, mortality, and economic
cost. The continuous emerging of bacterial resistance to antibiotics worsens the
situation and complicates the challenges. The epidemiology of these infections is well
studied in developed countries, but the picture is not that clear in developing
countries. The neonatal septicemia is reported in Gaza and connected to mortality, but
the epidemiology of neonatal septicemia was never studied.
Objectives: The research aimed to study the epidemiology of neonatal septicemia by
defining the main etiological bacterial agents of it in the neonatal intensive care units,
the potential predisposing factors for acquiring septicemia, the potential pathogenic
bacteria existed in the environment of the units, and the antibiotic resistance patterns
of isolated bacteria.
Methodology: A three-month descriptive cross-sectional study in two intensive care
units in Gaza city (Al-Shifa and Al-Nasser hospitals). The study consists of a
checklist to evaluate environmental and working conditions, a questionnaire to survey
the healthcare workers' knowledge and perspective, scanning patient's records for
potential risk factors, blood cultures for patients, sampling the environment and the
workers for potential pathogens and testing isolated microorganisms for antibiotic
susceptibility.
Results: A total of 622 cases, more than half of them from Al-Nasser hospital
(56.6%, n=346). The incidence rate of septicemia was 10.4% (24.2/1000 patient day)
in Al-Nasser unit (n=36), and 9.1% (14.4/1000 patient day) in Al-Shifa's (n=25). The
causative
bacteria
were:
coagulase-negative
Staphylococcus
(39%,
n=24),
ii
the least
resistance(27%).
Conclusions: Neonatal sepsis is not a risk factor for mortality. Apgar score <7,
birthweight less than 2.5 kg, preterm, inherited disorders and cesarean section
delivery are the risk factors.
Potential intrinsic risk factors for septicemia are: preterm, low birth weight and
gender (male). Maternal fever and meconium staining of amniotic fluid could be
predictive factors for septicemia in newborns.
Extended beta-lactamase producing gram negative bacteria may be associated to
resistance to quinolones. Resistance of Staphylococcus spp. to Meropenem is a
serious finding.
Adherence of healthcare workers to hand hygiene and personal protective procedures
beside appropriate disinfection of the environment are key factors to reduce the
acquisition of neonatal septicemia and other infections. This may be achieved by
promotion, role modeling and continuous monitoring. Besides that, the availability
and accessibility of alcoholic hand-rub solutions will make the difference.
Keywords: epidemiology, neonatal sepsis, Gaza, Palestine, infection control,
nosocomial.
iii
:
. .
, .
, .
:
,
, ,
.
:
) ( . ,
, ,
, ,
.
: 622 , ) .(%56.6
24.5) %10.4 1000 ( ) 36( , %9.1
) 14.4 ( ) 25( . 24 :
) 14 ,(%39 ) 7 ,(%23 )5 ,(%12
, 5 ) %8 ( 3 , 3 ) %5
(.
, , .
.
)( .
) ,(%53 )(%27
: ,
> ,7 2.5 , , .
iv
, )(.
.
.
.
,
.
.
: , , , , , ,
Declaration
"I hereby declare that this submission is my own work and that, to the best of
my knowledge and belief, it contains no material previously published or
written by another person nor material which to a substantial extent has been
accepted for the award of any other degree of the university or other institute,
except where due acknowledgment has been made in the text".
Yasser A. Elbayoumi
Copyright by
Yasser A. Elbayoumi
2011
Copyright.
All Right Reserved: No part of this work can be copied, translated or stored in
retrieval system, without prior permission of the author.
vi
DEDICATION
vii
List of contents
Declaration ...........
Dedication .................
List of contents
List of figures..
List of tables ...........
List of annexes
List of abbreviations...
Acknowledgments ......
vi
vii
viii
xi
xi
xi
xii
xiii
CHAPTER I: INTRODUCTION
1.1 Overview ........................
1.2 Objectives .......................
1.3 Significance .........
1
4
4
2.1 Introduction .
2.2 Bloodstream infections (BSI) in neonates .
2.2.1 Laboratory-confirmed bloodstream infection (LCBI) ...................
2.2.2 Clinical sepsis (CSEP) ...
2.3 Etiology and rates of infection ..
2.3.1 Etiological agents ...
2.3.1.1 Gram positive bacteria ...
Group B Streptococcus (GBS) ....
Staphylococcus aureus ....
Coagulase-negative staphylococci ..
Enterococcus species ..
Group A, C, D, and G Streptococcus species .
Listeria monocytogenes ..
2.3.1.2 Gram-Negative Organisms
Escherichia coli ..
Enterobacter, Klebsiella, and Serratia species ..
Citrobacter species .
Pseudomonas ..
Acinetobacter species .
Haemoplilus influenzae ..
2.3.1.3 Anaerobic Bacteremia ...
2.3.1.4 Fungal sepsis ..
2.3.2 Infection rates
2.3.3 Mortality rates
2.4 Acquisition of Infection .
2.4.1 Colonization of the Newborn .
2.4.2 Modes of Transmission ..
2.4.2.1 Direct contact transmission
2.4.2.2 Indirect contact transmission
2.5 Risk Factors for Infection ...
viii
5
6
7
8
8
8
8
8
8
9
9
10
10
10
10
11
11
12
12
13
13
14
14
15
16
16
18
18
19
20
21
22
23
24
24
25
26
26
28
28
28
29
29
30
30
32
33
36
36
36
37
37
37
38
38
38
38
39
39
39
40
40
40
40
40
41
41
41
42
42
CHAPTER IV Results
43
43
44
44
44
45
45
45
45
45
46
47
47
49
50
50
50
50
54
54
54
54
54
55
55
CHAPTER V: Discussion
58
59
60
64
65
65
66
66
67
67
68
69
72
75
77
77
78
104
List of figures
Fig 2.1: Timing of bacterial and fungal sepsis in VLBW infants .
Fig 3.1: Sampling of nasal swab ...
Fig 3.2: Sampling of hand swab
Fig 3.3: Sampl'air: Air sampler for microbiological samples ...
Fig 4.1: Photographs of Handwashing facilities in NICUs ..
Fig 5.1: The role of workers in directing towards personal hygiene practices
PHP as evaluated by health care workers (questionnaire results) .
Fig 5.2: Isolated bacteria from Environment and healthcare workers and blood
cultures
Fig 5.3: Use and resistance patterns of frequently administered antibiotics in the
two NICUs ...
7
40
40
41
44
62
68
72
List of tables
Table (3.1): Microbiological samples from the two NICUs
Table (4.1): Distribution of Al-Shifa cases according to gender and mode of
delivery
Table (4.2): Relation between mortality rate and maternal and neonatal factors
(calculated for both NICUs cases) ...
Table (4.3): Symptoms classification according to nursery care level .
Table (4.4): Neonatal and maternal factors in neonates with clinical sepsis (AlNasser hospital) ...
Table (4.5): Neonatal and maternal factors in neonates with septicemia (positive
blood culture)
Table (4.6): Antibiotic administration in Al-Nasser and Al-Shifa NICUs
according to hospitals records ...
Table (4.7): Distribution of the questionnaire respondents according to
profession and gender .
Table (4.8) Isolated bacteria from different sources in the two NICUs
Table (4.9): Sources of tested bacterial isolates for antibiotic susceptibility
Table (4.10): Antibiotic susceptibility patterns (%) for bacteria isolated from
different sources from Al-Nasser and Al-Shifa NICUs .. ..
39
46
47
48
48
49
50
50
55
56
56
List of annexes
Annex 1: Environmental and working conditions checklist .
Annex 2: Al-Nasser NICU environmental swabs .
Annex 3a: Al-Shifa NICU environmental swabs (ground floor) .....
Annex 3b: Al-Shifa NICU environmental swabs (first floor) .........
Annex 4: Perception Survey for Health-Care Workers ......................................
Annex 5: Perception Survey for Health-Care Workers (in Arabic) ...................
Annex 6: Environmental and working conditions checklist results ..
Annex 7: Results of the perception survey ...
Annex 8: Results of air samples of NICU of Al-Nasser and Al-Shifa hospitals ..
Annex 9: Antibiotic sensitivity for selected Gram negative bacteria isolated
from blood culture, environment, hand and nasal swabs ...
Annex 10 : Antibiotic sensitivity of staphylococcus aureus isolates ....
Annex 11: Antibiotic sensitivity of Al-Shifa NICU Coagulase negative
Staphylococcus (CoNS) .......
Annex 12: Antibiotic sensitivity of Al-Nasser NICU Coagulase negative
Staphylococcus(CoNS) .....
xi
104
108
109
110
111
112
113
117
118
119
120
121
122
List of abbreviations
AAP
ASPs
BHIB
BSI
CAH
CDC
CHNRI
CLABSIs
CLSI
CMV
CNS
CoNS
CRP
CSEP
DRBC
ELBW
EMRO
EONI
EONS
ESBL
GBS
HAI
HAV
HBV
HCV
HCW
HIV
HSV
HTLV-I
ICPs
ICU
IFI
LCBI
LONS
MMWR
MRSA
MSAF
NEC
NI
NICHD
NICU
NNIS
PCBS
PHP
PNR
SIRS
SPSS
VLBW
VLONS
VRE
WHO
xii
Acknowledgment
I would like to express my gratitude to all people who have contributed to this work.
In particular, I would like to thank:
Special thanks to my supervisor Dr. Abedelraouf Elmanama, for his
professionalism, encouragement and enthusiastic. He is a true researcher driven by
curiosity and with never ending energy. Without his stimulating, critical discussions,
comments, and great help, this work would not have been completed.
To the professors, Dr. Yousef Abu-Safieh and Dr. Basim Ayesh for their precious
advises. Their contributions have strengthened and enriched the content of this work.
To my colleagues in the public health lab. for their support, help and encouragement
in all stages of this work. Among them, Mohammed Seada, Hashim Arafa, Asaad
El Falit, Mohammed El Khatib and Saleh El Tawil were of great help.
Special thanks to my dear colleagues Ms. Ohoud Sarsour and Mr. Nahedh
Abdullatif for their kind and appreciable help.
To the workers of the microbiology laboratory and the archives at Al-Shifa and AlNasser hospitals for their significant help, without it, this work would have never been
accomplished. Also the workers of the NICUs in the two hospitals, where their
cooperation had an effective role in facilitating this work.
I would like also to thank all my friends and colleagues, for all of their support and
guidance and encouragement.
Finally, special thanks and apologies to my family: beloved wife, dear brothers and
sisters, and my sweet children . Without their guidance, help and patience, I would
have never been able to accomplish this work.
xiii
CHAPTER I
Introduction
1.1 Overview
At any point of time, over 1.4 million people worldwide are suffering from infections
acquired at hospitals. Between 5% and 10% of patients admitted to modern hospitals
in the developed world acquire one or more infections. The risk in developing
countries is 2 to 20 times higher [1]. In some developing countries, the proportion can
exceed 25% [2]. Infections are an important cause of neonatal morbidity and mortality
worldwide. Neonatal infections among low-birth-weight infants are associated with
significant risk of neurologic abnormalities, developmental and functional delays [3]
Although most neonatal infections are of maternal or community origin, an increasing
proportion are acquired in the nursery. Advances in newborn intensive care have
permitted the survival of low-birth-weight and sick infants and have simultaneously
created risks for neonatal infections, which are themselves a significant cause of
mortality in these infants [4]. Reported infection rates in the neonatal intensive care
unit (NICU) vary from 3.2 to 30 per 100 admissions or discharges, illustrating the
wide variability among centers. NICUs that admit surgery patients may have higher
rates [5]. Nosocomial bloodstream infections (BSIs) are increasing in prevalence and
result in significant morbidity, mortality, and economic cost. From 1975 to 1996, the
proportion of nosocomial infections accounted for by BSIs increased from 5% to 14%
[6].
Traditionally, three different categories of risk factors associated with nosocomial
infection (NI) acquisition have been described; factors inherent to patient, to invasive
procedures and to hospital environment. The study of these factors can guide the
selection, implementation, and evaluation of control measures for this type of
infection [7]. However, extensive investigations often fail to yield specific sources,
and the clusters may spontaneously disappear. This suggests that environmental or
host factors that have yet to be identified also contribute to the acquisition of NIs [4].
The centers for disease control and prevention (CDC) replaced the generic term
"nosocomial" with Health-care associated infection (HAI). The CDC defines an HAI
as a localized or systemic condition resulting from an adverse reaction to the presence
1
of an infectious agent(s) or its toxin(s). There must be no evidence that the infection
was present or incubating at the time of admission to the acute care setting [8]. The
world health organization (WHO) is less conservative than CDC in terminology;
Nosocomial infections, known also as hospital-acquired infections, hospitalassociated infections, and hospital infections [9] are infections that are not present in
the patient at the time of admission to hospital but develop during the course of the
stay in hospital [10]. In the coming chapters the definition "health-care associated
infection (HAI)" will be used.
There are two forms of infections; Endogenous infection, (self-infection, or autoinfection), in which the causative agent of the infection is present in the patient at the
time of admission to hospital but there are no signs of infection. The infection
develops during the stay in hospital as a result of the patients altered immunity. The
other form is cross-contamination followed by cross-infection; during the stay in
hospital the patient comes into contact with new infective agents, becomes
contaminated, and subsequently develops an infection [10]. While there is no
clinically significant difference between the endogenous self-infection and the
exogenous cross-infection, the distinction is important from the standpoint of
epidemiology and prevention [9].
In recent years, the subject of the emergence and subsequent increase in the incidence
of resistance to antimicrobial agents has become a serious threat. Reports from all
around the world suggest that antibiotics are rapidly losing their effectiveness, with
some early reports going so far as to suggest that we are approaching a post-antibiotic
era [11]. Antimicrobial resistance is increasing for a variety of reasons, these include
suboptimal use of antimicrobials for prophylaxis and treatment of infection, prolonged
hospitalization, increased number and duration of intensive-care-unit stays, multiple
co-morbidities in hospitalized patients, increased use of invasive devices and
catheters, ineffective infection-control practices, noncompliance with infectioncontrol practices, transfer of colonized patients from hospital to hospital, grouping of
colonized patients in long-term-care facilities, antibiotic use in agriculture, and
increasing national and international travel [12]. The rate of antimicrobial resistance
among HAI pathogens is steadily increasing; a 2000s surveillance revealed increasing
rates of MRSA, VRE, and other patterns of resistance patterns [13].
2
1.2 Objectives
The overall objective is to study the epidemiology of neonatal septicemia at the
selected NICUs. The following specific objectives will be achieved:
1. To evaluate the environmental and working conditions in two different NICUs
and their potential role in causing HAI.
2.
3.
To identify the potential bacterial pathogens in the environment and those carried
by the working staff of the units
4.
5.
1.3 Significance
Neonates are highly susceptible to NIs, due to their weak immune system. The
environmental and work conditions of the NICUs impose another risk factor, and can
be the major cause of infection.
The prevalence of many NIs in Al-Shifa NICU has been reported in the last decade,
few of them have been documented. The records of Al-Nasser pediatric hospital
showed that about one third of blood culture in a three-month period where from
NICU, and more than 20% of them were positive cultures, while less than 10% were
positive in other sections.
NIs extend the stay of neonates in the hospital, and raise the cost of treatment with
antibiotics. The results of this study may provide insight of the etiological agents of
septicemia and the associated risk factors. This would be of importance in planning
actions to reduce such infections.
CHAPTER II
Literature Review
2.1 Introduction
Infections are important cause of neonatal morbidity and mortality worldwide.
Although most neonatal infections are of maternal or community origin, an increasing
proportion are acquired in the nursery. Advances in newborn intensive care have
permitted the survival of low-birth-weight and sick infants and have simultaneously
created risks for HAI, which are themselves a significant cause of mortality in these
infants [4].
Prevention of infection in the premature infant who starts life in an intensive care unit
and whose immature defenses are further depleted by illness and invasive procedures
is a major challenge. The newborn may acquire infection from the mother in utero,
during delivery or postpartum from maternal, hospital, or community sources. Many
infections transmitted from mother to infant during delivery, such as group B
hemolytic streptococci (GBS), Listeria, hepatitis B virus (HBV), or herpes simplex
virus (HSV), have not traditionally been considered HAIs. On the other hand,
infections classified as HAIs are often caused by microorganisms acquired from the
mother that become part of the flora of the newborn and subsequently invade because
of immature or impaired defenses. Difficulty in distinguishing between maternal and
hospital sources makes identification of newborn HAIs imprecise. Because of this
difficulty, the Center for Disease Control and Prevention (CDC) has defined all
neonatal infections, whether acquired during delivery or during hospitalization, as
HAIs unless evidence indicates transplacental acquisition [21].
Most published reports of HAIs have included only those infections with onset within
a specified period after admission to the nursery, whereas some have attempted to
separately define infections from maternal and hospital sources. The need to
distinguish between maternal and hospital sources is more than semantic. Infection
control measures designed to prevent acquisition of microorganisms within the
nursery will not affect pathogens acquired prenatally, for which control measures
involve prevention, diagnosis, and treatment of infection in the pregnant woman;
5
Figure 2.1: Timing of bacterial and fungal sepsis in VLBW infants. Percentages indicate the
approximate number of VLBW infants with septicemia. EONS usually occurs via ascent of organisms
from the birth canal to the amniotic fluid, with or without rupture of amniotic membranes. LONS
occurs with vertical and horizontal spread of organisms. While the vast majority of cases of sepsis in
VLBW infants occur in the first 30 days of life, VLBW infants requiring prolonged intensive care are
at risk for VLONS beyond 2 months of age (23).
From a diagnostic perspective, CDC has defined two types of BSI; Laboratoryconfirmed bloodstream infection (LCBI), which may be used to report BSI in all age
groups, and clinical sepsis (CSEP), which may be used only to report primary BSI in
neonates and infants, but not in adults and children [8].
narrow-spectrum
-lactamaseresistant
antimicrobial
drugs
(e.g.,
methicillin, oxacillin) appeared soon after they were introduced into clinical
practice in the 1940s and 1960s, respectively [28].
NICUs, yet several studies have reported endemic or epidemic vancomycinresistant enterococci (VRE) among hospitalized neonates [30].
Escherichia coli: Since E. coli is the most common cause of neonatal sepsis by
gram-negative bacteria, both organism and host response have been investigated.
A number of E. coli virulence factors have been identified and linked to neonatal
10
epidemic outbreaks in both well-baby and intensive care nurseries. C. koseri is not
a normal inhabitant of the maternal urogenital tract, but it is occasionally present,
causing maternal UTI and chorioamnionitis. Vertical transmission may lead to a
neonate with severe sepsis at birth or in the first days of life [35]. Horizontal
transmission of C. koseri from patient to patient via the hands of infant caregivers
has been documented. In the early 1980s, a number of outbreaks of C. koseri
meningitis in well-baby nurseries were reported [36].
differences also occur and isolated studies in India and Pakistan have reported GBS to
be an important cause of early-onset sepsis. S. aureus is the most common pathogen
in African countries and a peculiar trend of Acinetobacter/Pseudomonas infections
was noted in Asia Pacific [51].
There are few data on infection rates in normal nurseries, where the infant is healthy
and the hospital stay is short. Reported rates are low, from 0.3 to 1.7 per 100
newborns. Infection rates in infants of birth weights less than 1,500 g, 1,501 to 2,500
g, and more than 2,500 g were 63%, 8.2%, and 6%, respectively in a study from the
USA, and 74%, 28%, and 13%, respectively in a study from Brazil [5].
National nosocomial infections surveillance (NNIS) system of the CDC rates for all
newborn nurseries reporting in 1984 were 0.9 and 1.7 per 100 discharges for
nonteaching and large teaching hospitals, respectively [52]. Reported infection rates
in the NICU in the following decades vary from 3.2 to 30 per 100 admissions or
discharges, illustrating the wide variability among centers [53]. NICUs that admit
surgery patients may have higher rates. A rate of 58 per 100 admissions was reported
in one small series from a newborn surgery unit [5].
2.3.3 Mortality rates
Neonatal mortality is increasingly recognized as an important global public health
challenge that must be addressed to reduce child health disparities between rich and
poor countries. Most of the estimated 4 million neonatal deaths per year occur in low
and middle income countries [54], in another measurement 99% in developing
countries [55], yet most epidemiological and other research focuses on the 1% of
deaths in rich countries [56].
Three conditions: infection, birth asphyxia, and consequences of premature birth/low
birth weight, are responsible for majority of these deaths. More than one-third is
estimated to be due to severe infections, and a quarter is due to the clinical syndrome
of neonatal sepsis/pneumonia. Case fatality rates for neonatal infections remain high
among both hospitalized newborns and those in the community [57].
15
According to WHO regional classification; the highest infant mortality rate (deaths in
1000 live births) in the year 2008 was in African region (40), while the lowest was in
European region (7). The Eastern Mediterranean region came second (35), the region
includes Arab countries, Iran and Afghanistan (occupied Palestine, Gaza strip and the
west bank are not included) [58]. In the Palestinian territories the rate is 25/1000 live
births [18].
Differences in mortality rates inside developed countries are reported as well, in a
study on sepsis-related mortality among newborns in the US, it was concluded that
despite declines in the overall mortality among newborns, racial and regional gaps in
mortality persisted over the 16-year study period (i.e. blacks and infants born in the
South) [59].
Preventing deaths in newborn babies has not been a focus of child survival or safe
motherhood programs. While these challenges are neglected, 450 newborn children
die every hour, mainly from preventable causes, which is unconscionable in the 21st
century [56]. It is no longer possible to overlook the important contribution of
neonatal mortality to overall infant survival. To reduce neonatal mortality caused by
infections, a strong case must be made for investment in expanded surveillance
activities and in further research on diagnosis, etiology, and optimal management of
neonatal sepsis at all levels of the health system [60]. The Department of Child and
Adolescent Health and Development of the World Health Organization (WHO/CAH)
applied the Child Health and Nutrition Research Initiative (CHNRI) priority-setting
methodology to identify and stimulate research most likely to reduce global newborn
infection-related mortality by 2015 and concluded that the implementation of research
studies in developing countries on health systems and policy research are top priority
to accelerate reduction of neonatal deaths, particularly due to infections [61].
2.4 Acquisition of Infection
2.4.1 Colonization of the Newborn
The neonatal period is crucial for intestinal colonization, and the processes involved
in the establishment of microbial populations are complex and involve both microbial
succession as well as interactions between the infant and the microbes in the different
16
anaerobic
bacteria,
such
as
staphylococci,
streptococci
and
Enterobacteriaceae [66].
Antibiotic administration results in suppression of all anaerobic bacteria, with the
exception of clostridia, which remain at detectable levels, and increased numbers of
Klebsiella,
Enterobacter,
Citrobacter
and
Pseudomonas.
Lactobacilli
and
17
Shared toys are bacterial reservoirs [82], and may become a vehicle for
transmitting pathogenic bacteria such as Pseudomonas aeruginosa [83] or
respiratory viruses such as respiratory syncytial virus (RSV) [84] among
pediatric patients.
19
Clothing and uniforms such as white coats [88], isolation gowns [89], gloves
when contaminated [90] or leaked [91] when used as personal protective
equipment (PPE), may become contaminated with potential pathogens after
care of a patient colonized or infected with an infectious agent such as MRSA
[92], VRE [93], and C. difficile [94].
Many other vectors and reservoirs have been reported in the health care environment,
(e.g., computer hardware [95], rings [96], keyboards [97], doctors neckties [98],
mobile phones [99], soap dispensers [100] and wristwatches [101]). Water sources are
additional potential hazards in the NICU. Blood transfusions may be a source of
viruses such as cytomegalovirus (CMV), Hepatitis A, B and C viruses (HAV, HBV,
HCV). Breast milk is another source of blood-borne viruses. Approximately one third
of CMV-seropositive women excrete CMV in their breast milk, and two thirds of
these women were found to transmit CMV to their newborns by breast-feeding. HIV
is transmitted from mother to newborn by breast milk, and breast-feeding may be the
major means of acquisition of human T-cell leukemia virus type I (HTLV-I). Breast
milk may contain bacteria if the mother is bacteremic or has mastitis but is more
likely to be contaminated with bacteria during collection or handling. One study
reported growth of gram-negative bacilli in 36% of samples of unpasteurized human
milk. Formula feeds may also become contaminated during preparation or handling.
Contaminated blenders have been identified as a source of infection. Bacteremia and
meningitis have been associated with powdered infant formula intrinsically
contaminated with Enterobacter sakazakii [5].
2.5 Risk Factors for Infection
HAI rates on different neonatal units vary widely. There are several reasons for this
variation, including differences in the way that sepsis is defined, differences in the
types of babies treated and differences in standards of care. There is clear evidence
that the contributors to HAI are indeed multifactorial. Clusters of infection with
particular nosocomial pathogens inevitably occur on NICUs from time to time. An
understanding of risk factors for acquisition and/or infection with the outbreak strain
can inform infection control measures to terminate the outbreak [102].
20
The determination of risk factors for all-cause sepsis is the most useful approach,
where the aim of surveillance is to compare intra- or inter-unit infection rates, since
the predominant microbial flora in units varies. The only exception to this might be
CoNS, which account for the majority of blood culture isolates in NICUs. Infection
rates with these bacteria might, therefore, represent a reasonable proxy for overall
infection rates. However, such an approach might mask important differences in rates
of infection with less common, but more virulent, pathogens [103].
Risk factors for BSI fall into three main categories:
1. Intrinsic risk factors that cannot be influenced, and relate to the patients biological
status. Some such risk factors are static, for example, birth weight, gestational age and
condition at birth, whereas others, for example, postnatal age, vary daily.
2. Extrinsic risk factors that relate to treatment that the individual patient receives.
These risk factors may vary from day to day.
3. Risk factors that relate to infrastructural considerations, such as access to
handwashing and isolation facilities, environmental cleanliness and staffing numbers.
These consist of a mixture of static and variable elements [102].
21
Natural killer cell activity, important in control of herpes group viral infections, is
also decreased [105].
It is universally agreed that the incidence of late onset sepsis is inversely proportional
to birth weight and gestational age [102]. The incidence of preterm births (<37 weeks
gestation) is increasing in many countries around the world and has become a global
health concern. More than 70% of preterm infants are born between 34 and 36 weeks
gestation (late preterm). Most large series describing the epidemiology of neonatal
sepsis are limited to infants with very low gestational age (<33 weeks) or VLBW
(<1500 g birth weight) [106].
Maternal risk factors can be included in this category; maternal fever, pre-labour
rupture of membranes of >18 hours, premature onset of labour, chorioamnionitis,
urinary tract infections and group B streptococcus (GBS) colonization are the key
maternal risk factors [51]. The effect of gestational age on the risk of GBS disease for
example could be explained by the amount of maternal IgG antibodies received by the
infant, because susceptibility to invasive GBS disease has been correlated with
deficiency in levels of maternal type-specific serum IgG antibodies [107].
2.5.2 Extrinsic risk factors (Invasive Procedures)
Any procedure that disrupts the normal barriers to infection is likely to present a
higher risk of infection in the newborn than later in life. The normal newborn escapes
most invasive procedures but may be subjected to scalp electrodes or percutaneous
punctures for blood sampling. Scalp electrodes provide a portal of entry for maternal
genital microorganisms. Infectious complications occur in less than 1% of infants and
most are benign abscesses, but severe cellulitis, bacteremia, osteomyelitis, and
disseminated HSV infection have been reported. Premature and ill newborns often
require feeding by nasogastric tubes, which provide a portal of entry and potentiate
overgrowth of microbes in the upper gastrointestinal tract. Breast milk and formula
feeds administered by continuous infusion remain at room temperature for several
hours, allowing microbes to proliferate in the reservoir or tubing during infusion.
[108]. The most commonly reported causative pathogens of central lineassociated
bloodstream
infections
(CLABSIs)
remain
22
CoNS,
Staphylococcus
aureus,
enterococci, and Candida spp. Gram negative bacilli accounted for 19-21% of
CLABSIs reported to CDC [109].
23
surveillance. All culture positive patients in hospital are evaluated for a possible HAI
or a community acquired infection. The cut-off of a two to three day interval between
hospitalization and a positive bacterial culture is used to identify HAI. Every
suspected case of HAI is reviewed for confirmation. The HAI rate is computed
monthly as episodes per 100 hospital admissions. Nevertheless, the limited approach
of laboratory culture-based surveillance could be realistic, with negligible financial
burden on the hospital management [123].
Logically, surveillance should begin only after all recommended steps for preventing
HAIs have been taken. For hospitals in most countries, rigorously employing the
evidence-based infection prevention practices should be the primary strategy for
preventing NIs and avoiding bad outcomes in hospitalized patients. Then the use of
measures proven to reduce infection risk at specific sites or from invasive procedures
should be checked. Only after successfully implementing and monitoring these
recommendations should the use of surveillance be considered [121].
recognize and analyze problems, to effectively target infection control measures and
feedback. Any suspicion of an outbreak should lead to a review of general infection
control procedures to prevent the spread of the pathogens as quickly as possible. A
multidisciplinary approach can be an effective means of developing a plan of action to
apply prolonged and strict adherence to isolation precautions, to detect potential
reservoirs or source of infections, to educate every member of the patient care team
and to review NICU protocols [126].
2.6.3 The role of the microbiology laboratory
The microbiology laboratory has become an integral part of a hospital epidemiology
and infection control program. The constantly changing spectrum of nosocomial
pathogens and their susceptibilities and the availability of newer technologies require
constant communication, cooperation, and collaboration between microbiology
personnel and infection control personnel (ICPs). In the twenty-first century, this
relationship is more critical than at any time in the past [127]. The clinical
microbiology laboratory contributes to preventing transmission of infectious diseases
in healthcare settings by promptly detecting and reporting epidemiologically
important organisms, identifying emerging patterns of antimicrobial resistance, and
assisting in assessment of the effectiveness of recommended precautions to limit
transmission during outbreaks, outbreaks of infections may be recognized first by
laboratorians [128]. Today, however, the work done by the microbiology laboratory is
increasingly complex and demanding. Much of this has direct implications on hospital
epidemiology and infection control. Microbiology laboratories now must be able to
detect, identify, and characterize an expanded array of microbes, including newly
emerging pathogens [127].
2.6.4 Environmental monitoring
Microbiologic sampling of air, water, and inanimate surfaces (i.e., environmental
sampling) is an expensive and time-consuming process that is complicated by many
variables in protocol, analysis, and interpretation. It is therefore indicated for only
four situations [129]:
Critical Items: Critical items confer a high risk for infection if they are
contaminated with any microorganism. Thus, objects that enter sterile tissue or
the vascular system must be sterile because any microbial contamination could
transmit disease. This category includes surgical instruments, cardiac and
urinary catheters, implants, and ultrasound probes used in sterile body cavities.
Most of the items in this category should be purchased as sterile or be
sterilized with steam if possible. Heat-sensitive objects can be treated with
ethylene oxide, hydrogen peroxide gas plasma; or if other methods are
unsuitable, by liquid chemical sterilants [136].
28
Noncritical Items: Noncritical items are those that come in contact with intact
skin but not mucous membranes. Intact skin acts as an effective barrier to most
microorganisms; therefore, the sterility of items coming in contact with intact
skin is "not critical". Noncritical items are divided into noncritical patient care
items and noncritical environmental surfaces [139]. Examples of noncritical
patient-care items are bedpans, blood pressure cuffs, crutches and computers
[97]. In contrast to critical and some semicritical items, most noncritical
reusable items may be decontaminated where they are used and do not need to
be transported to a central processing area. Virtually no risk has been
documented for transmission of infectious agents to patients through
noncritical items [136]. Noncritcal environmental surfaces include bed rails,
some food utensils, bedside tables, patient furniture and floors. Noncritical
environmental surfaces frequently touched by hand (e.g., bedside tables, bed
rails) potentially could contribute to secondary transmission by contaminating
hands of health-care workers or by contacting medical equipment that
subsequently contacts patients [140]. Mops and reusable cleaning cloths are
regularly used to achieve low-level disinfection on environmental surfaces.
However, they often are not adequately cleaned and disinfected, and if the
water-disinfectant mixture is not changed regularly (e.g., after every three to
four rooms, at no longer than 60-minute intervals), the mopping procedure
actually can spread heavy microbial contamination throughout the health-care
facility [141]. Frequent laundering of mops (e.g., daily), therefore, is
recommended. Single-use disposable towels impregnated with a disinfectant
also can be used for low-level disinfection when spot-cleaning of noncritical
surfaces is needed [136].
these molecules through the 1970s and 1980s allowed us to believe that we could
always remain ahead of the pathogens. By the turn of the century this complacency
had come to haunt us. The pipeline of new drugs is running dry and the incentives to
develop new antimicrobials to address the global problems of drug resistance are
weak. Antimicrobial use is the key driver of resistance. Paradoxically this selective
pressure comes from a combination of overuse in many parts of the world,
particularly for minor infections, misuse due to lack of access to appropriate treatment
and underuse due to lack of financial support to complete treatment courses [146].
A drug-resistant organism may be introduced into a health care facility with the
admission of a patient who is infected with or who has been colonized by such a
strain. Alternatively, antimicrobial resistance may emerge in bacteria as a response to
selective antibiotic pressure, or a resistant organism may spread from person to
person. Often, a combination of these factors may be involved in the emergence and
transmission of antimicrobial resistance within a health care facility [147].
The role of antibiotic exposure on the acquisition of antibiotic resistant bacteria in the
intensive care nursery is difficult to calculate given the covariance of such exposure to
other markers of severe disease. Experience has demonstrated, however, that use of
the aminoglycosides is infrequently associated with emergence of resistance in the
newborn, whereas the use of higher-generation cephalosporins may be associated with
the rapid appearance of bacilli resistant to -lactamses [148]. The extraordinary
genetic capacities of microbes have benefitted from man's overuse of antibiotics to
exploit every source of resistance genes and every means of horizontal gene
transmission to develop multiple mechanisms of resistance for each and every
antibiotic introduced into practice clinically, agriculturally, or otherwise [149].
Selective antibiotic pressure enhances the risk of transmission by increasing a
patients' bacterial load (through selection of preexistent resistant flora), with a
subsequent risk of hand contamination in health care workers, and by creating new
ecological niches for resistant flora after eradication of susceptible flora in other
patients [150].
Hospital-based data show alarming rates of resistance to Ampicillin and Gentamicin
among common pathogens causing neonatal sepsis (71% of Klebsiella and 50% of
Escherichia coli are reportedly resistant to Gentamicin), suggesting that the WHO
31
three pathogens appears to be less common in Africa, but data are insufficient. There
are important regional differences in susceptibility patterns of Haemophilus
influenzae and pneumococci in Africa, with some countries (South Africa, Malawi)
reporting high resistance rates to penicillin, chloramphenicol and cotrimoxazole; other
African countries have intermediate (Kenya, Senegal), or low resistance rates
(Gambia, Central African Republic, Ghana). There is a substantial resistance among
respiratory pathogens to cotrimoxazole in South Asia [51].
2.7.4 Antimicrobial resistance control
Information regarding antimicrobial resistance among infections-causing bacteria in
communities is essential for developing appropriate management strategies. In
addition, the sustainability of community-based management strategies depends on
monitoring changes in the etiology as well as resistance patterns of serious infections
over time. Unfortunately, there is a paucity of information on resistance patterns of
community-acquired infections in neonates and young infants in developing countries,
owing to lack of appropriate laboratory and susceptibility testing facilities and
challenges of conducting studies of etiology of serious infections in community
settings [154]
In the present battle against the rising tide of resistance, several interventions have
been proposed to help control the situation. One of these is a process of planned
antibiotic restriction, introduced through cycling drug selection based on local
surveillance. Although such antibiotic cycling has been the subject of much
discussion, there are relatively few data available to assess its worth [155]. Cycling or
rotation is the scheduled substitution of a class of antibiotics (or a specific member of
a class) with a different class (or a specific member of that class) that exhibits a
comparable spectrum of activity. This substitution may be followed after a fixed
interval by a third, fourth or, indeed, any number of substitutions, but the cycle must
be repeated, with re-introduction of the original class/drug [156]. A dilemma may
exist in regard to replacing an antibiotic that is losing effectiveness due to resistance
with a new drug within the same class. Such replacement may enhance treatment
success in the short term but promote the spread of highly resistant strains [157]. A
one year study on 1062 infants found no detectable effect of antibiotic cycling in
decreasing the reservoir of resistant Gram-negative bacilli in a tertiary-care NICU
33
[158]. Moreover, it's believed that cycling is unlikely to be effective and may even
hinder resistance control. Alternative drug-use strategies are suggested such as
mixing, in which each treated patient receives one of several drug classes used
simultaneously in the hospital [159].
Antimicrobial stewardship programs (ASPs) promote the appropriate use of
antimicrobials by selecting the appropriate dose, duration, and route of administration.
The appropriate use of antimicrobials has the potential to improve efficacy, reduce
treatment-related costs, minimize drug-related adverse events, and limit the potential
for emergence of antimicrobial resistance [160]. At this time, data from wellcontrolled studies examining the effect of ASPs on emergence of resistance are
limited, but available data suggests that good ASP reduces rates of C. difficile
associated diarrhea, resistant gram-negative bacilli, and vancomycin-resistant
enterococci [161].
In addition, using pharmacokinetics and pharmacodynamics principles to guide
antimicrobial dosing regimens may have a role in controlling development of
resistance. Enforcing rigorous infection control practices can reduce the transmission
of problematic pathogens within the healthcare setting [162]. Nevertheless, a strategy
whereby multiple or all classes of antibiotics are available for use (i.e., antibiotic
heterogeneity) can be part of a broader effort aimed at curtailing antibiotic resistance
within ICUs. Such efforts should be routine, given the limited availability of new
antibiotic drug classes for the foreseeable future [163].
Strategies should also be adopted to reduce antibiotic consumption in NICUs, a
randomized controlled trial found no evidence that routine antibiotic use has a
protective effect in low risk preterm neonates [164]. On the other hand, there is also
clear evidence that in the management of patients with severe infection, not only must
the chosen antibiotic regimen be appropriate, but its administration must be promptly
initiated [165]. The importance of early initiation of appropriate antibiotic therapy
was confirmed in an analysis of patients with sterile-site MRSA infections. In this
retrospective analysis of 549 patients treated over a 3-year period through the end of
2004, appropriate antibiotic therapy initiated within the first 24 h after collection of a
culture-positive specimen was correlated with a significantly higher survival rate
34
(33.4% vs. 22.0% among those who did not receive appropriate antibiotics; P = .015)
[166]. Rapid laboratory tests such as Interleukin-8 (IL-8) and/or C-Reactive Protein
(CRP) can reduce unnecessary antibiotic therapy and is cost-effective [167].
To achieve complete restitution of therapeutic applications of antibiotics, there is a
need for more information on the role of environmental microbiomes in the rise of
antibiotic resistance. In particular, creative approaches to the discovery of novel
antibiotics and their expedited and controlled introduction to therapy are obligatory
[149].
In conclusion, the frequencies of resistant bacteria in hospitals can be reduced by (i)
reducing antibiotic use, (ii) controlling the spread of bacteria, (iii) using antibiotics for
which there is no resistance, (iv) increasing the rate of turnover of patients, and (v)
restricting the input of patients and health-care workers carrying resistant nosocomial
pathogens [145]. The design of antimicrobial management programs should be based
on the best current understanding of the relationship between antimicrobial use and
resistance. Such programs should be administered by multidisciplinary teams
composed
of
infectious
diseases
physicians,
clinical
pharmacists,
clinical
35
Chapter III
Materials and Methods
3.1 Materials
3.1.1 Apparatus
Manufacturer (Country)
Air sampler
Autoclave
Tuttnauer (USA)
Colony counter
Anderman (UK)
Deep freezer
Kirsch (Germany)
Digital camera
Incubator
Carbolite (France)
Optical microscope
Zeiss (Germany)
Refrigerator
Sanyo (Italy))
Water bath
36
Potency
10 units
10 g
100 g
30 g
5 g
30 g
10 g
30g
10 g
10 g
5 g
30 g
5 g
30 g
30 g
30 g
15 g
Abbreviation
P
Am
PIP
Cn
Cfm
Cro
GM
Ak
I
MEM
TR
Va
Cp
Na
C
Te
E
Manufacturer- Country
HiMedia- India
HiMedia- India
HiMedia- India
Oxoide-UK
Oxoide-UK
Difco- USA
Difco- USA
HiMedia- India
HiMedia- India
HiMedia- India
Oxoide-UK
Oxoide-UK
Difco- USA
Oxoide-UK
HiMedia- India
HiMedia- India
Difco- USA
37
3.2 Methodology
A cross-sectional descriptive study consists of a checklist to evaluate environmental
and working conditions, a questionnaire to evaluate the healthcare workers'
knowledge and perspective, scanning patient's records for potential risk factors, blood
cultures for patients, sampling the environment and the workers for potential
pathogens and testing isolated microorganisms for antibiotic susceptibility.
3.2.1 Permission and ethical consideration
Permissions were obtained from the general administration of hospitals, hospitals
administration and heads of the selected NICUs (annex 13).
3.2.2 Environmental and working conditions
A checklist was designed to evaluate the environmental and working conditions of the
NICUs included in this study (Al-shifa and Al-Nasser) (annex 1). The 1st part is an
overview of the unit describing the work and treatment areas, the working staff, the
environmental conditions, the infrastructure maintenance and monitoring beside the
antimicrobial therapy regimen. The 2nd part describes formation, role and activities of
the infection control team. The 3rd part covers the handwashing and personal hygiene
which describes handwashing basins, personal protection equipment, handling and
disposal of sharps beside the intravascular access devices (catheters). The 4th part
covers the cleaning processes describing the routine environmental cleaning, the
management of clinical wastes, the management of blood and body spills beside the
use and cleaning of trolleys.
3.2.3 Hospital records
Data of admitted cases were obtained from the hospitals archives which are noncomputerized; each case has a separate file with a serial number. The file includes:
name of the newborn, date of birth, date of admission, birth weight, mode of delivery,
Apgar score, primary diagnosis, date and state of departure, administered medications,
prognosis of the case, laboratory test results, maternal age and parity, physicians notes
and nurses diaries. Data were collected for all admitted cases in a three-month period
(April - June 2010)
38
AlShifa
25
19
19
70
26
159
AlNasser
36
18
18
40
14
126
Total
61
37
37
110
40
285
39
b- Environmental samples
Sterile swabs filled with 3 ml of BHIB were used to swab approximately 10 cm2 [170]
of each environmental spot (tested spots are detailed in annexes 2, 3). Swabs were
then incubated overnight at 37o C and tested for turbidity. Positive samples (turbid)
were subcultered on Blood and MacConkey agars and incubated overnight at 37o C.
c- Nasal samples
Sterile swabs were used to collect nasal
samples by inserting the swab in one side of
participant nose and rolling it gently (figure
3.1) [171]. 3 ml of BHIB were added to the
swab tube to cover the sample. Swabs were
then incubated over night at 37o C and tested
40
overnight at 37o C. Positive samples (turbid) were subcultered on Blood agar and
MacConkey agar and incubated overnight at 37o C.
e- Air samples
An
air
sampler
(Sampl'air-
AES
41
42
CHAPTER IV
Results
4.1 Environmental and working conditions
A predefined checklist was used to evaluate the environmental and work condition of
the NICUs included in this study. The findings of the checklist are summarized in
annex (6). The findings of the checklist showed that the two hospitals lack defined
documentation systems in nearly all fields. The importance of documentation is not
stressed in the managerial systems of the hospitals.
4.1.1 Work and treatment areas
The location of the NICUs differs in the two hospitals; at Al-Shifa hospital, although
the unit is physically connected to the delivery section, it is well isolated from other
sections. At Al-Nasser hospital, the unit lacks this advantage, besides that, the traffic
flow is more facilitated in Al-Shifa NICU.
Infant space in both units is less than 2 m2, with a maximum distance of about or less
than 1 m between incubators. Handwashing sinks are less than 1 m far from the
closest incubator. No measures are taken to prevent water splashing or retaining
(figure 4.1). The use of sinks is not clearly defined, mixed use in Al-Nasser NICU,
and no clear signs to restrict them for handwashing only. No air filtration or
ventilation is provided in the two NICUs, but temperature is controlled using air
conditioning system. The dining area is physically separated in Al-Shifa NICU, while
the dining table is located exactly in the middle of the main ward in Al-Nasser NICU.
43
Figure 4.1: Photographs of Handwashing facilities in NICUs; left: Al-Shifa , right: Al-Nasser
locations in the hospital. Dealing with outbreaks seems to be the main cause for the
formation of the teams, microbiologists play crucial role in this field.
4.1.5 Personal protection equipment (PPE)
Gloves, masks, gowns, aprons and protective footwear are available in different
kinds, but not used or not properly used at all times.
4.1.6 Handling and disposal of tools
No written instructions are available, sharps are passed between HCW by hand in AlNasser NICU, but claimed to be passed by sharp trays at Al-Shifa NICU. Sterile
equipment are stored in a clean dry environment and well protected. Sharp disposal
containers are labeled and puncture proof. Thermometers are cleaned and disinfected
each use.
both governmental and private, while Al-Shifa NICU cases came exclusively from the
delivery department at the same hospital, which is physically connected to the NICU,
so it was important to compare numbers of admitted cases to the total delivery cases
at the hospital. The distribution of the total number of cases according to gender and
mode of delivery is shown in table (4.1), which clearly illustrate that male and
Caesarean section delivered neonates are more likely to develop morbidities.
Table (4.1): Distribution of Al-Shifa cases according to gender and mode of delivery
Gender
Male
Female
2151
1865
Total
170
106
NICU cases
(7.9%)
(5.7%)
(%)
P=0.003**
Statistical
OR=0.70
significance
NICU= Neonatal Intensive Care Unit
Mode of delivery
Vaginal
C. section
3085
931
141
135
(4.6%)
(14.5%)
P= <0.0001**
OR=3.5
** p =0.01
Total
4016
276
(6.9%)
4.2.1 Mortality
The total number of deaths at Al-Shifa NICU was 72 cases distributed according to
primary diagnosis as follows: Respiratory distress (n=55, 76.4%), Preterm (n=39,
54.2%,), Abortion (n=5, 6.9%), Polycystic kidney (n=3, 4.1%), (Hydrocephalus,
Asphyxia, Pulmonary hypertension) (n=2 each, 2.8%), (Spina bifida, Sepsis,
Osteogenesis
Hepatomegaly,
imperfecta,
Hernia,
Meningomyelocele,
Gastrochiasis,
Esophageal
Pulmonary
atresia,
hemorrhage,
Thalassemia,
Potter
46
Table (4.2): Relation between mortality rate and maternal and neonatal factors (calculated for both
NICUs cases).
Statistical significance
Parameter
Variables
Total Deaths (%)
P value
Odds Ratio
377
48 (12.7)
Male
0.262
0.83
Gender
Female
214
32 (15.0)
369
19 (5.1)
Term
0.0001**
0.14
Gestation age
Preterm
215
60 (27.9)
221
45 (20.4)
3 days
0.021*
1.68
Hospitalization period
>3 days
289
35 (12.1)
409
45 (11.0)
Vaginal
0.006**
0.52
Mode of delivery
C. section
177
34 (19.2)
199
62 (32.6)
Normal
0.0001**
10.71
Birth weight
Low
370
15 (4.1)
66
48 (72.7)
<7
0.0001**
240.9
Apgar score
7
274
3 (1.1)
554
67 (12.1)
No
0.0001**
0.23
Inherited disorder
Yes
35
13 (37.1)
534
71 (13.3)
Positive
Septicemia (blood
0.361
0.81
Negative
57
9 (15.8)
culture)
186
3 (1.6)
Yes
0.22
0.45
Sepsis
No
140
5 (3.6)
62
7 (11.3)
< 20 years
0.54
1.03
Maternal age
20 years
437
48 (11)
154
16 (10.4)
Multi
0.54
1.03
Parity
premier
292
30 (10.3)
* p < 0.05 , ** p <0.01
Apgar score, birth weight, gestation age and inherited disorders showed a very high
effect on mortality rate, followed by mode of delivery and hospitalization period.
Sepsis (clinically diagnosed) seems to have an effect (OR=0.45) but the p value was >
0.05. Maternal factors (age and parity) have no effect.
4.2.2 Clinical sepsis (CSEP) and Laboratory-confirmed infection (LCBI)
Relation between CSEP and LCBI was assessed for Al-Nasser cases only, since it was
almost absent as a primary diagnosis in Al-Shifa records (4/276, 1.45%). The
correlation was highly significant (p=0.001, OR=3.4); 16.7% of sepsis cases were
positive for blood culture (25/150), while only 5.6% of other cases were positive
(11/196).
4.2.3 Risk factors for mortality and septicemia
The level of nursery care for admitted cases depends on the primary diagnosis. Higher
care levels usually include more invasive procedures (central lines, mechanical
ventilation, etc) which may impose another risk factor for HAI. This factor was
studied in order to evaluate the effect of invasive procedures which were not well
47
documented in the records. After consulting pediatricians at the NICUs, the cases
were divided into 2 categories as shown in table (4.3)
Table (4.3): Symptoms classification according to nursery care level
Care
Symptoms
level
Preterm
gestational age (SGA), Transient tachypnea of the newborn (TTN), Fever, Dehydration,
Average
Hypoglycemia, Vomiting, Diabetic Mother (IDM), HB mother, Mecon staining, Sepsis, Cyanosis,
Wet lung, ABO incompatibility Hepatomegaly, Polycystic kidney, Down syndrome, Hematoma,
Anemia, Thalassemia, Bleeding, Pallor, Skin infection, Hypocalcaemia, Lower limb edema,
Bronchitis, URTI, Omphalitis, Convulsion, seizure
Preterm ( 28 weeks), Family history of Pompe, Spina bifida (post op.), Cloacal exstrophy (post
op.), Hernia (post op.), Esophageal Artesia (post op.), Pyloric stenosis (post op.) Respiratory
distress syndrome, Asphyxia, Intestinal obstruction, Low birth weight, Encephalopathy, Abortion,
High
encephalopathy
(HIE), Septic shock, Meningitis, Congenital Heart Disease (CHD), Pneumonia, Transposition of
the Great Arteries (TGA), Inborn error of metabolism.
Post op. = post operation
Risk factors for CSEP were measured only from the records of Al-Nasser NICU
(CSEP is absent from Al-Shifa records) (table 4.4), while risk factors for LCBI for
each unit are summarized in table (4.5)
Table (4.4): Neonatal and maternal factors in neonates with clinical sepsis (Al-Nasser hospital)
Parameter
Variables
Male
Gender
Female
Term1
Gestation age
Preterm2
3 days
Hospitalization
>3 days
period
Vaginal
Mode of delivery
C- section
Normal
Birth weight
Low
<7
Apgar score
7
< 20 years
Maternal age
20 years
Multi
Parity
Premier
1
1
>37 weeks, 2 37 weeks
Suspected
sepsis (%)
Total
cases
Statistical significance
P value
Odds Ratio
222
0.346
1.12
124
291
0.042*
0.54
48
224
0.0001**
2.3
122
283
0.332
0.84
56
272
1.95
0.032*
47
10
0.565
0.90
177
43
0.559
0.99
279
211
0.049*
1.56
98
* p < 0.05 , ** p <0.01
94 (42.3)
56 (45.2)
133(45.7)
15(31.3)
81(36.2)
69(56.6)
124(43.8)
23(41.2)
126(46.3)
14(29.8)
5(50)
84(47.5)
19(44.2)
123(44.1)
98(46.4)
35(35.2)
48
The highest effect on sepsis was for hospitalization period, followed by birth weight,
gestation age and maternal parity. No effects were found for gender, mode of
delivery, Apgar score and maternal age.
Table (4.5): Neonatal and maternal factors in neonates with septicemia (positive blood culture)
Hospital NICU
Al-shifa
Al-Nasser
Variables
Parameter
+ve1 Total Stat. sigin.2
+ve1 Total Stat. sigin.2
22
170
P=0.003**
26
222
P=0.186
Male
Gender
Female
3
106
OR=0.2
10
124
OR=0.66
5
122
P=0.008**
19
224
P=0.082
0-3 days
Hospitalization
>3 days
20
153
OR=3.52
17
122
OR=1.74
period
5
104
P=0.066
33
291
P=0.215
Term3
Gestation age
Preterm4
20
178
OR=2.35
3
48
OR=0.52
11
141
P=0.297
31
283
P=0.400
Vaginal
Mode of delivery
C- section
14
135
OR=1.37
5
56
OR=0.77
21
166
P=0.008**
2
47
Normal
P=0.100
Birth weight
Low
4
109
OR=0.26
32
272
OR=2.93
7
60
P=0.438
2
10
P=0.312
<7
Apgar score
7
11
113
OR=0.82
19
177
OR=0.48
4
61
P=0.313
28
276
P=0.419
Average
Care level
High
21
215
OR=1.54
8
68
OR=1.18
1
20
P=0.485
5
43
P=0.544
< 20
Maternal age
20
16
184
OR=1.81
31
279
OR=0.95
4
64
P=0.367
12
98
P=0.494
Multi
Maternal parity
premier
9
99
OR=1.50
22
211
OR=0.83
1
Positive, 2Statistical significance, 3>37 weeks, 4 37 weeks
** p <0.01 OR= Odds Ratio
Based on chi square tests, only gender, hospitalization period and birth weight have
affected the incidence of septicemia in Al-Shifa cases and no such risk factors in AlNasser cases. Odds Ratios change the view; gestation age can be added as approved
risk factor beside maternal age to some extent. In Al-Nasser cases birth weight and
Apgar score are approved factors beside gestation age to some extent.
Other risk factors can be discussed; maternal fever and mecuonium staining of
amniotic fluid (MSAF) are not highly documented in the records, but out of 7
documented cases of maternal fever, only one was submitted to blood culture and it
was positive, and out of four documented cases of MSAF, only one case was
submitted to blood culture and it was positive.
4.2.4 Antibiotic administration rates
The primary option of antibiotic prophylaxis is Ampicillin followed by Gentamicin or
a combination of both given to the most of admitted neonates. The other antibiotics
49
Mean4
3.47
2.41
1.68
0.93
0.28
0.06
Al-Shifa
F Total
3
2
5
7
6
13
10
18
Al-Nasser
Total
F
5
0
5
9
5
14
8
16
2
11
Total
10
27
14
24
13
37
19
Total
Responses for the seventeen questions are summarized in annex (7). Less than half of
the respondents (48.6%) have received recent training about personal hygiene and
50
51
About half of the respondents (52.8%) couldnt evaluate the commitment of their
colleagues to personal hygiene practices (PHP) (19/36), the others gave estimates
from 30% to 90% with an average of 66.8%.
About one third of the respondents (35.1%) couldnt evaluate their own commitment
to PHP (13/37). The others gave estimates from 30% to 100%, with an average of
67.8%.
More than half of the respondents (54.1%) described the role of infection control
committee as low or very low (n=20), 32.4% described its role as moderate (n=12),
13.5% described its role as important (n=5) and none of them described its role as
very important, with no statistically significant relation to profession (p=0.367) or
working experience (p=0.920), but it was apparently unpopular among females
(p=0.025).
It was important to compare respondents evaluation of the committees in the two
hospitals. In Al-Nasser NICU, 57.9%, described its role as low or very low (n=11),
the others 42.1% (n=8) described it as moderate, none described it as high or very
high. In al-Shifa NICU, the infection control committee has relatively more respect,
27.8% described its role as high (n=5), the others varied from moderate (22.2%, n=4),
low or very low (50%, n=9). The difference between hospitals was statistically
significant (p=0.039)
About half of the respondents (51.5%, n=19) believed that HAI negatively affects the
patient prognosis, 32.4% believed the effect is moderate (n=12), the others believed
the effect is low (16.2%, n=6), with no statistically significant relation to profession
(p=0.205), gender (p=0.211), or working experience (p=0.058).
The vast majority of respondents (86.5%) believed that handwashing is highly
effective in preventing HAI (N=32), only 13.5% didn't agree (n=5), with no
statistically significant relation to profession (p=0.123), gender (p=0.668), or working
experience (p=0.123).
52
In the evaluation of direct managers role in directing workers to PHP, 36.2% of the
respondents evaluated it as low or very low (n=13), the same number evaluated it as
high or very high, 27.8% of them evaluated it as moderate (n=10), with no statistically
significant relation to profession (p= 0.551), gender (p=0. 823), or working
experience (p=0.351).
In the evaluation of colleagues role in directing workers to PHP, 35.1% of the
respondents evaluated it as low or very low (n=13), the same number evaluated it as
moderate, 29.7% of them evaluated it as high or very high (n=11), with no statistically
significant relation to profession (p= 0.519), gender (p=0. 875), or working
experience (p=0.180).
In the evaluation of workers role in directing residents (patients and companions) to
PHP, 32.4% of the respondents evaluated it as low or very low (n=12), 37.8% of them
evaluated it as moderate (n=14), 29.7% of them evaluated it as high or very high
(n=11), with no statistically significant relation to profession (p= 0.492), gender (p=0.
376), or working experience (p=0.484).
In the evaluation of residents (patients and companions) role in directing workers to
PHP, 62.2% of the respondents evaluated it as low or very low (n=23), 27% of them
evaluated it as moderate (n=10), only 10.8% of them evaluated it as high (n=4), with
no statistically significant relation to profession (p= 0.543), gender (p=0. 480), or
working experience (p=0.595). It is worth mentioning that a significant difference
(p=0.014) was found between hospitals.
With regard to the best way to make workers commit to PHP, respondents gave 53
answers (the possibility of picking more than one answer raised the number).
Promotion was the first option (54.8%, n=29), role model came second (20.4, n=11),
while enforcement came last (17%, n=9), four of the respondents gave other
suggestions, the first one was punishment of non-complying workers, the second
suggestion was "conscious", the third was the continuous education of workers, the
last one was the continuous monitoring.
53
Pantoea spp. (5%, n=6), E. coli, and S. rubidaea (2%, n=2 each), P. mirabilis and
Errwinia sp. (1%, n=1 each).
4.4.5 Air microbial load
Bacterial and fungal counts are summarized in annex (8). The bacterial count mean in
Al-Nasser NICU was about 1740 cfu/m3, in Al-Shifa NICU, it was about 1680 cfu/m3.
The fungal count mean in Al-Nasser NICU was about 480 cfu/m3, while in Al-Shifa
NICU it was about 520 cfu/m3. Some of the dominant bacterial colonies in the plates
were identified; main isolates were: CoNS, Bacillus spp., Pseudomonas spp.,
Aeromonas sp. and Actinomycetes.
Table (4.8) Isolated bacteria from different sources in the two NICUs.
Hospital NICU
Isolate source
Al-Nasser
A
B
E
H
N
T
CoNS
4 17 8
3
2
34
Staphylococcus aureus
0 10 0
3
4
17
Streptococcus sp.
0
5
0
0
0
5
Bacillus sp.
5
0
3
5
1
14
Klebsiella pneumonia
0
0
2
2
0
4
Escherichia coli
0
0
0
0
1
1
Enterobacter aerogenes
0
0
1
0
0
1
Enterobacter cloacae
0
2
4
0
0
6
Enterobacter sakazakii
0
0
3
0
0
3
Pantoea sp.
0
0
4
1
0
5
Citrobacter freundii
0
0
4
0
1
5
Proteus mirabilis
0
0
0
0
0
0
Serratia rubidaeae
0
0
1
0
1
2
Acinetobacter sp.
0
0
2
0
0
2
Pseudomonas sp.
4
2
6
3
6
21
Aeromonas sp.
0
0
3
0
0
3
Erwinia sp.
0
0
1
0
0
1
Actinomycetes
2
0
0
0
0
2
Total
15 36 42 17 16 126
A=air, B=blood, E= environment, H= hand, N=nasal, T=total
A
6
0
0
5
0
0
0
0
0
0
0
0
0
0
2
1
0
3
17
B
7
4
2
0
3
3
0
3
0
0
0
0
0
0
3
0
0
0
25
Al-Shifa
E
H
N
4
3
7
0
0
5
0
0
0
7
4
0
7
2
0
2
0
0
9
0
0
7
1
0
7
1
2
2
2
0
6
2
1
1
0
0
1
0
1
11
2
2
2
0
0
4
0
0
0
0
0
0
0
0
70 17 18
T
27
9
2
16
12
5
9
11
10
4
9
1
2
15
7
5
0
3
147
55
T
61
26
7
30
16
6
10
17
13
9
14
1
4
17
28
8
1
5
273
A
6
6
Al-Shifa NICU
B
E
H
N
7
4
3
7
5
5
2
1
1
2
7
1
2
2
1
16 15
5
14
T
27
10
4
10
5
56
T
52
32
16
15
5
120
S. aureus
K. pneumoniae
E.cloacae
E. coli
Penicillin G
Ampicillin
Piperacillin
Cephalexin
Cefixime
Ceftriaxone
Gentamicin
Amikacin
Imipinem
Meropenem
Trimethoprim
Vancomycin
Chloramphenicol
Tetracycline
Erythromycin
Ciprofloxacin
Nalidixic acid
Average
NT=not tested
CoNS
Isolate \
Antibiotic
Gram negative
Average
(n=52)
0
6
100
65
33
48
77
81
100
17
53
100
92
85
19
87
NT
62
(n=32)
0
3
100
44
6
50
31
81
100
44
41
100
78
75
80
84
NT
57
(n=16)
NT
0
6
0
13
44
31
94
100
100
25
NT
69
50
NT
75
57
47
(n=15)
NT
7
80
7
54
80
80
87
100
100
60
NT
87
87
NT
100
87
73
(n=5)
NT
20
40
20
20
20
40
100
100
100
20
NT
100
60
NT
40
40
51
(n=120)
00
13
66
33
26
49
51
93
100
73
39
100
85
71
50
77
61
58
The highest resistance is for K. pneumoniae (53%), and the lowest is for E. cloacae
(27%) (resistance is calculated by subtracting the suscibtibility percentage from 100).
High resistance against penicillins is found for both gram positive and gram negative
bacteria, Piperacillin is the exception where it was highly active against gram positive
bacteria and E. cloacae, but not K.pneumoniae or E.coli. The three generations of
cephalosporins shown relative weak activity against all tested bacteria, the second
56
57
CHAPTER V
Discussion
The aim of this research was to study the epidemiology of neonatal septicemia in local
hospitals in order to define the best ways to interrupt the cycle of infection. An
environmental checklist and perspective questionnaire were introduced to define
environmental and human role in the cycle. In addition, the environment and working
staff were sampled to compare the microbial flora of the healthcare environment with
the etiologic agents of neonatal septicemia. The patient's hospital records were
scanned to define potential neonatal and maternal risk factors. Antimicrobial
susceptibility of some of the isolated bacteria from different sources was tested to
evaluate the role of antibiotic prophylaxis and treatment in the dynamics of the
problem.
5.1 Incidence and prevalence of neonatal septicemia
The limitations of the diagnosis of bloodstream infections among neonates motivated
the CDC to introduce the term clinical sepsis (CSEP) to be used for neonatal
septicemia beside the all-age term laboratory confirmed bloodstream infection (LCBI)
[8, 21]. To assess the efficacy of diagnosis in the studied units, the relation between
CSEP and LCBI was measured. The CSEP diagnosis was almost absent from AlShifa records which may be due to misdiagnosis or to records deficiency, while in ANasser it was well documented as "septicemia" or "sepsis" as a primary diagnosis.
About half of the cases (n=150, 44%) were primarily diagnosed as sepsis. Although a
high significance was calculated for Al-Nasser unit (p=0.001, OR=3.4), this finding
can be misleading because only 16.7% of suspected sepsis was laboratory approved.
The fact that clinical signs and laboratory data have not been perceived as sensitive or
specific for early stages of sepsis [174] could explain this finding. At Al-Shifa unit,
out of the four suspected sepsis cases, three produced positive blood culture, but the
fourth case wasnt subjected to the test. This emphasizes the importance of restoring
"all-case blood culture" strategy.
Calculated from the total deliveries at Al-Shifa hospital, sepsis rate is 6.23/1000 live
birth, which is lower than the rate in Gaza in 2004 (12.8/1000) [175], and higher than
the rate in southern occupied Palestine (3.2/1000) [176], and close to the rate in all
58
occupied Palestine (6.13/1000) [177] and USA (5.16/1,000) [178], and to the lower
limit in Asia (7.1-38/1000), Africa (6.5-23/1000) and to the mean rate in south
America and the Caribbean (3.5-8.9/1000) [143]. The current study reveals a
considerable decrease in neonatal sepsis from 2004 to 2010 in Gaza which may be
due to the efforts done after repeated outbreaks in 2004 [15,16]. The coincidence of
repeated outbreaks during the study of El Jadba and El Yazji could be a bias factor
when considering another study at the same period [14] where 4.1% rate was found
for HAI in general.
LCBI rate in Al-shifa unit was 9.1% (14.4/1000 patient day), and 10.4% (24.2/1000
patient day) in Al-Nasser's. The difference between the two units could be due to the
restricted blood culture strategy in Al-Shifa unit and the less controlled environmental
conditions in Al-Nasser unit compared to Al-Shifa's (an outbreak of K. pneumoniae
took place in Al-Nasser unit immediately after completion of sampling for the current
study). Unlike incidence rate, the use of patient day denominator elaborates the
difference between the two units, this finding support the suggestion of Chen et al.,
[179] to use this denominator in reporting the incidence of occupational exposures in
the healthcare facilities.
CoNS incidence, although decreased since 2004 (57%) [175], is still dominant among
etiological agents of LCBI (39%), K. pneumoniae and Pseudomonas spp. retained the
same incidence with a decrease in E. coli. The outbreak bacteria (Serratia and
Acinetobacter) have disappeared. These results are not far from other reported results
in the occupied Palestine [180]. CoNS was not always as dominant as the current
period in our region, Enterococuus was reported to be the main gram positive causing
neonatal bacteremia in an earlier report in occupied Palestine [181]. This fact reflects
the importance of continuous surveillance.
5.2 Occupational and infrastructural risk factors
Understaffing, overcrowding and poor hygiene practices are key factors in HAI
[111,182-191].
59
compliance with infection control measures. Objectivity was assured; estimates were
60
about 68% and 67% for the two questions respectively. Additionally, these findings
reflects tendency among HCW to admit their incompliance with infection control
measures contrary to Boyce who concluded that self-reporting of compliance is not
sufficiently reliable to be useful [118]. This tendency may be a good baseline for a
productive approach to enhance compliance; passive deviance (PD) is based on the
observation that in every community there are certain individuals or groups whose
uncommon behaviors and strategies enable them to find better solutions to problems
than their peers, while having access to the same resources and facing similar or
worse challenges [201]. This approach was used recently to improve compliance
among HCW to PHP at a private tertiary care hospital in Brazil, and resulted in
measurable increase in handwashing and decrease in the incidence of HAIs [202],
sustainability in improvement in hand hygiene was also confirmed in another report
for the same authors [203].
Communication in this field is important; creating a culture where reminding each
other about hand hygiene and use of gloves is encouraged makes compliance the
social norm. Figure (5.1) represents the evaluation of HCW of the role of
communication in the units: from managers to staff (Q14), from staff to their
colleagues (Q15), and from staff to residents (patients and/or companions) (Q16)
(annex 7).
61
Fig 5.1: The role of workers in directing towards personal hygiene practices (PHP) as evaluated by
health care workers (questionnaire results)
Q14- The role of managers in directing workers to PHP
Q15- The role of colleagues in directing workers to PHP
Q16- The role of workers in directing residents to PHP
The equal distribution of the opinions from low to high and the low numbers of
determined opinions (very low and very high) represents the lack of a consensus
among HCW, which may be resulting from lack of interest. The absence of
institutional commitment to hand hygiene may be derived from these findings. The
absence of planned training programs, and monitoring (annex 6) supports this
conclusion. Institutional commitment to hand hygiene practice is an important factor
in the continuous effort for enhancing workers' commitment [118].
Differences
can transfer the knowledge to others in the section, and the presence of such person in
the section will be a continuous motivation for others.
Infection control teams should support ICU personnel in their efforts to upgrade
facilities and help ensure that this is a priority when resources are limited [207]. This
cannot be achieved unless a good relation is established between infection control
personnel and HCW. According to HCW (annex 7, Q11), infection control teams are
not doing a good job, this may be due to poor communication and lack of facilities.
Infection control strategies should be centrally directed, and each team should
implement tailored programs based on central strategies of the health administration.
The statistically significant difference in the evaluation of Al-Shifa team over AlNasser's (p=0.039) (annex 7, Q11) gives the impression that the strategies are locally
designed and remote hospitals are far from administration follow up and monitoring.
The evaluation of HCW of the teams can be confirmed by the findings of the checklist
(annex 6); Al-Shifa`s team is more organized, includes more professions, and have a
separate headquarter in the hospital. In fact, both teams are newly assigned and
enough time should be given before final evaluation.
It is becoming clear that patients must be part of any meaningful solution to the
challenges facing health care [208]. Continuous quality improvement focuses on the
customer and, therefore, requires attention to customers feedback as a vital input
[209]. The role of patients and companions in directing HCW towards personal
hygiene was underscored by the HCW themselves (annex7-Q17), 27% of them even
denies the right of the patients to interfere (annex7-Q4). The relation between HCW
and healthcare receivers should be evaluated and patients role should be strengthened
in directing HCW towards the adherence to infection control measures. Public
performance reports, particularly those that highlight high and low performers, push
hospitals to improve [210]. Patient opinion websites [211] are now of important value
in this direction. Although it is complicated by conflicting attitudes, intentions, and
behaviors of patients and health care professionals toward engagement in safety issues
[212], patient participation has become increasingly recognized and advocated as the
key component in the redesigning of health care processes to enhance patient safety
63
[213]. Public awareness of their role is the best way to enforce these practices, and
their role, to my mind, should be enforced by law.
5.2.2 Environmental conditions
Environmental cleaning in the studied NICUs (annex 6) is done in a routine manner
for floors, walls, windows and curtains as mentioned by senior cleaners, but
disinfection of the environment is not receiving enough attention. The absence of
written instructions for environmental cleaning, management of spills and
management of clinical wastes indicates low attention and makes it very hard to
monitor and to evaluate the process. This could be the direct reason for the absence of
monitoring of environmental conditions (annex 6). Lack of ventilation and air
filtration in the units are additional risks contributing to environmental contamination
(annex 6).
Appropriate cleaning and disinfection programs are essential to render the ICU
relatively pathogen free and compliance with handwashing is imperative in
minimizing infection in this high-risk area [207]. There is an increasing body of
evidence that cleaning or disinfection of the environment can reduce transmission of
healthcare-associated pathogens [214].
procedures have been proved to be not enough for full eradication of HAI pathogens
[215-217], hence, improved methods of disinfecting the hospital environment are
needed [214]. Moreover, cleanliness is not enough to assure effective removal of
pathogens and visual assessment is not a reliable indicator of surface cleanliness or of
cleaning efficacy [215,218].
Dining area in Al-Shifa NICU is separated from the wards, but in Al-Nasser NICU,
the table is located in the center of the main ward and is used for dining beside other
uses (e.g. reports filling), which contradicts with the basic rules of infection control.
Workflow differs significantly between the two units. All five wards in Al-Shifa unit
are well separated from each other, while in Al-Nasser's, the three wards open into
each other (the only way to the main ward passes through reception and then
resuscitation room).
64
65
66
solid agars to avoid overlooking potential pathogens which exist in low numbers but
still impose risk.
5.3.2 Air microbial load
The availability of an air microbial sampler was the incentive for choosing this
method over the air sedimentation method which is more frequently used [245-249].
There are no standardized methods for bacterial air sampling or its frequency. Most of
the industrialized countries set their own standards, usually modifying the American
Federal Standard 209E to their local needs [250]; The American Federal Standard
adopted particulate count for evaluation purposes and didnt mention the microbial
count [251]. The only standard (after extensive online research) was from Hong
Kong [252]; according to Hong Kong indoor air quality management group [253], the
total bacterial count and fungal count in indoor environment of offices and public
places shouldnt exceed 500 cfu/m3. In healthcare facilities, the limits should be more
restricted; In well ventilated operating theaters, bacterial count shouldnt exceed 50150 cfu/m3 [250]. In the studied units of the current study, bacterial counts range
(1260-2160 cfu/m3) is far above standards for public spaces, not to mention the
hospital environment. The fungal counts are not far from the standards (360-600
cfu/m3). Nevertheless, the results demonstrated relative excellence for Al-Shifa unit
over Al-Nasser's. lack of ventilation or air filtration in both units may be the reason
for high microbial numbers.
5.3.3 Health care workers
Methods for the isolation of bacteria from the skin and particularly the hands have
included stripping with cellophane tape [254], swabbing small areas within glass
cylinders [255], imprinting fingertips on agar plates [256], rubbing with glass beads
within plastic bags or test tubes [257,258], scrubbing hands in basins [259], and
washing or rinsing methods [260] including glove-juice method [261]. Electric
toothbrushes were also used [262].
According to the European standard, only the fingertips are sampled, as they have a
higher density of bacteria than all other parts of the hand [263], whereas according to
the U.S. standard, the whole hand is sampled [264]. Campf et al. found no difference
67
between the two test methods for the efficacy on the resident hand flora [265]. Rotter
et al. proved that the European method is effective and reproducible [266].
Choosing the European test method for this study was based on cost effectiveness and
ease, since fingers rubbing in a Petri dish is more acceptable for workers than glove
juice method, which is also time and materials consuming.
The advantages of using a swab in the nares compared to nasopharyngeal aspirate are
for the patient less discomfort, more rapid sampling procedure and lower cost [267].
5.3.4 Bacterial isolates
Figure 5.2 shows the relation between bacteria isolated from the environment and
HCW, and from the neonatal blood cultures.
Fig 5.2: Isolated bacteria from Environment and healthcare workers (dark), and blood cultures (light)
The figure reflects considerable similarities between bacteria isolated from the
environment and HCW (potential sources) and from blood cultures. This finding may
be a strong indicator for the role of environment and HCW as potential sources of
septicemia in neonates. Solid based evidence for this correlation should be based on
molecular typing, which is beyond the resources of the current work.
Three exceptions to this finding should be mentioned from the figure: Streptococcus
spp. K. pneumoniae, and Pseudomonas spp.
Streptococcus spp. is commonly maternally originated [26], and is not commonly
isolated from environments of healthcare facilities [268,269]. K. pneumoniae
68
(p=0.042, OR=0.52) and LCBI (p=0.066, OR=2.35 for Al-shifa, and p=0.215,
OR=0.52 for Al-Nasser) doesnt have the same strength in regard to chi square test.
For chi square test to give significance, numbers in the four fields should be above 5,
thats why Odds Ratio was used and gave important significance. In Al-Nasser unit,
preterm labor seems to be a protective factor for CSEP and LCBI. The nature of the
admitted neonates could be the reason for this finding where most of preterm infants
in the unit belong to late preterm category (34-37 weeks) and only 4 cases belong to
early preterm category (<34 weeks). Putting in mind that most large series describing
the epidemiology of neonatal sepsis are limited to infants with very low gestational
age [106] supports this explanation.
Normal birthweigh (2.5kg) was predictive for mortality (p=0.0001, OR=10.91),
CSEP (p=0.032, OR=1.95) and LCBI in Al-Shifa unit (p=0.008, OR=0.26). Only in
Al-Nasser unit low birthweight (<2.5kg) was predictive for LCBI (p=0.100,
OR=2.93). Most low birthweight cases in the current study dont belong to the very
low birth weight (VLBW) (<1.5kg) or extremely low birthweight (ELBW) (<1kg),
which are more predictive for mortality and morbidity [295,296]. Hospital level
where newborns are delivered may affect mortality and morbidity of low birthweight
newborns [296] which may explain the relation between LCBI and low birth weight
in Al-Nasser unit where infants are coming from lower level hospitals than Al-Shifa;
every preterm newborn in Al-Shifa hospital is transferred immediately to NICU.
Cesarean section delivery was found to be predictive of morbidity (table 4.1) and
mortality (table 4.2), but neither to CSEP (table 4.4) nor to LCBI (table 4.5). Many
researchers related cesarean section to some morbidities and to mortality [297-299],
while others demonstrated its protective effect [300]. Only repeated cesarean section
was connected to sepsis [301,302], a factor which is not well documented in the
studied records.
The cut-off point of 7 for Apgar score was used because no significant deference
between 0-3 and 4-6 groups [303]. Score < 7 was found to be extremely predictive
for mortality (p=0.0001, OR=240.9), but had no relation to CSEP (p=0.565,
OR=0.90) or to LCBI in Al-Shifa unit (p=0.313, OR=1.54) and some significance in
Al-Nasser unit (p=0.312, OR=0.48). The absence of significant relation between
LCBI and mortality (table 4.2) may confirm these findings. Low Apgar score is
71
proven predictive of mortality and morbidity [303-305]. Our findings contradict the
finding of Soman et al., [306] and Shah et al., [307], but both of them studied early
onset sepsis, while most of sepsis cases in the current study are late onset sepsis.
Absence of maternal factors effect on sepsis (tables 4.4, 4.5) could be explained by
the preponderance of late onset over early onset sepsis. Maternal fever and meconium
staining of amniotic fluid (MSAF) although under-documented seem to be exceptions.
Absence of invasive procedures from patient records lead to the use of care level as a
potential factor where high care level would be accompanied with more invasive
procedures. The significance of average care level to CSEP (table 4.4) is not useful,
since sepsis belongs to average care level category, LCBI was not connected to care
level (table 4.5) although invasive procedures are globally agreed to be of significant
prediction of LCBI.
5.5 Antimicrobial Use and Resistance
The use of antibiotic in the studied units is summarized in Table (4.6), and the results
of antibiotic sensitivity are summarized in table (4.10), and detailed in annexes (9-12)
Ampicillin, Gentamicin and Cefotaxime (claforan) and Amikacin to some extent are
more frequently used in the two units (table 4.6). Although complying with WHO
recommendations for antibiotic prophylaxis [51,308], the resistance among tested
bacteria seems to be a direct outcome of this compliance (fig 5.3).
Figure 5.3: Use and resistance patterns of frequently administered antibiotics in the two NICUs
72
New ESBL enzymes families are rising which presents great therapeutic challenges
for the 21st century [319].
ESBL is not uncommon in the Middle East and North Africa , it was reported in
southern occupied Palestine at the beginning of this century [320], and earlier in Saudi
Arabia [321], Tunisia [322] and Morocco [323], and later in Gaza strip [324].
Antibiotic choice is particularly important in seriously ill patients with infections due
to ESBL-producing K. pneumoniae. The use of a carbapenem (primarily imipenem)
was associated with a significantly lower mortality than was the use of other
antibiotics active in vitro [325]. Ertapenem is another good choice [326] and
tigecycline could be an option [327].
ESBL is indeed a serious threat; plasmids carrying ESBL genes frequently carry
aminoglycoside, tetracycline, sulfonamide or fluoroquinolone resistance genes [328].
Even the resistance to the strong combination piperacillin-tazobactam is thought to be
connected [329].
Quinolones (ciprofloxacin and nalidixic acid) are not frequently used in the two units
(table 4.6). Despite that, some resistance against ciprofloxacin and nalidixic acid is
found for K. pneumoniae and E. coli (table 4.10). The coexistence of quinolones
resistance
and
pneumoniae [330] and E. coli [331]. The two resistance mechanisms are thought to be
transferred on the same plasmid [332]. Putting in mind that ciprofloxacin resistance is
class effect, affecting all fluoroquinolones [333], makes the problem of greater
importance. Ciprofloxacin resistance was reported in Gaza in urinary tract infections
[334], but was not correlated to ESBL. This correlation should be confirmed through
molecular techniques.
Monitoring multidrug-resistant organisms and the infections they cause in a
healthcare setting is important to detect newly emerging antimicrobial resistance
profiles, to identify vulnerable patient populations, and to assess the need for and
effectiveness of interventions [335]. The current study could be an input in this
direction, and emphasize the importance of good monitoring of drugs.
74
CHAPTER VI
Conclusions and Recommendations
6.1 Conclusions
Neonatal septicemia is a very concerning health problem, healthcare environment has
a very important role in developing septicemia among neonates. Congregating sources
and susceptible targets for infections in the same area makes it very important to
understand the infection cycle and to define all direct and indirect contributing
factors. This is the only way to design appropriate measures to break the infection
cycle and to prevent (or to decrease) unwanted outcomes. One of the most annoying
obstacles in this issue is the continuous emerging of resistant microorganisms, which
raises the challenge for healthcare designers, providers and receivers.
The current study is a modest trial to contribute to this noble target. Two of neonatal
intensive care units in Gaza hospitals were extensively studied to define extrinsic and
intrinsic factors for neonatal septicemia.
The following conclusions were drawn from the study:
Potential risk factors for mortality include: Apgar score, birthweight of less
than 2.5 kg, preterm, inherited disorders (congenital diseases), and cesarean
section delivery.
Many healthcare workers were shown to harbor potential pathogens and thus
may be a likely source of infections.
75
Similar bacteria were isolated from the blood culture of the neonates and from
the units environment on the level of genus and species.
Important environmental differences related to workflow design between Alshifa and Al-Nasser NICUs raise the need for more attention and monitoring
of remote hospitals.
Hospitalization for more than 3 days was found to be predictive for morbidity
(including septicemia).
Potential intrinsic risk factors for septicemia are: preterm, low birth weight
and gender (male).
Among tested bacteria for antibiotic resistance, K. pneumoniae has shown the
highest rate of resistance, while E. cloacae has shown the least resistance;
despite that, alarming levels of resistance are detected.
76
6.2 Recommendations
In light of the results of this study, and the above-mentioned conclusions, the
following recommendations may be valuable in reducing the risks for septicemia and
other infections in the NICU:
1. Active and continuous surveillance program for infections in these hospitals
should be employed.
2. Infection control measures should be centrally designed, and should be
monitored and enforced among HCW.
3. More attention should be paid to disinfecting environmental surfaces and
monitoring the efficacy of the process.
4. Handwashing facilities should be monitored, maintained and supplied with
appropriate disinfectant soaps
5. Hand-rub alcoholic solutions should be available for all workers.
6. Periodical screening for environments (sterility testing) should include HCW,
and should be used for surveillance for prevalence of pathogens in the
environment and trends of antibiotic resistance profiles.
7. Separating dining areas from working areas.
8. Reviewing antimicrobial prophylaxis and treatment regimens based on local
antibiotic resistance patterns.
6.3 Research recommendations.
The findings of the current work raised some questions; the answers for these
questions may be the aims of future research work:
1. Correlation of bacteria isolated from the environment to those isolated
from infections using molecular techniques.
2. The prevalence of ESBL producing gram negative bacteria in the
environment and among infectious pathogens.
3. The incidence of Meropenem resistance among gram positive bacteria.
77
References
1.
Pittet D. and Donaldson L., 2006- Clean Care is Safer Care: a worldwide
priority. The Lancet; 366: 1246-1247
2.
3.
Vohr B.R., Wright L.L., Dusick A.M., et al., 2000- Neurodevelopmental and
Functional Outcomes of Extremely Low Birth Weight Infants in the National
Institute of Child Health and Human Development Neonatal Research Network,
19931994. Pediatr.; 105 (6): 1216 -1226
4.
Zafar N., Wallace M., Kieffer P., et al., 2001- Improving survival of vulnerable
infants increases neonatal intensive care unit nosocomial infection rate. Arch.
Pediatr. Ado. Med., 155:1098-1104.
5.
6.
7.
Arantes A., Carvalho E., Medeiros E., et al., 2003- Use of statistical process
control charts in the epidemiological surveillance of nosocomial infections. Rev.
Sade Pblica, 37 (6).
8.
Horan T., Andrus M. and Dudeck A., 2008- surveillance definition of health care
associated infection and criteria for specific types of infections in the acute care
setting. Am. J. Infec. Cont., 36:309-32.
9.
WHO, 1999- Hospital hygiene and infection control. In: Prss A., Giroult E.
and Rushbrook P., Safe management of wastes from health-care activities, WHO,
Hong Kong, p148-158 .
10. Ducel G., Fabry J., and Nicolle L., 2002- Prevention of hospital-acquired
infections, A practical guide, 2nd ed. WHO, Malta, p 1-64
11. Cohen M., 1992- Epidemiology of drug resistance: implications for a postantimicrobial era. Sci., 257: 1050-5.
12. Osmon D., 2001- Antimicrobial Resistance: Guidelines for the Practicing
Orthopaedic Surgeon. J. Bon. Join. Surg., 83:1891-1901.
78
13. Diekema D., Miller B., Vaughn T., et al., 2004- Antimicrobial resistance trends
and outbreak frequency in United States hospitals. Clin. Infect. Dis., 38:78-85.
14. Al Afifi A., 2005- Prevalence of multidrug resistant bacteria in nosocomial
infection MSc thesis, AlAqsa university. (Unpublished thesis).
15. Al Jarousha A., El Qouqa I., El Jadba A. , Al Afifi A., 2008- Acinetobacter
baumannii Infection in the Neonatal Intensive Care Unit. J. Pub. Heal., 37(3) :
107112.
16. Al Jarousha A., El Qouqa I., El Jadba A., Al Afifi A., 2008- An outbreak of
Serratia marcescens septicemia in neonatal intensive care unit in Gaza City,
Palestine. J. Hosp. Infect., 70(2): 119-126.
17. Awad N., 2009- Adherence to infection prevention & protection practices in the
Neonatal Intensive Care Units in the governmental hospitals in Gaza
governorates, Al Quds university. (Unpublished thesis).
18. East Mediterranean Regional Office (EMRO). 2010- country profile: Palestine,
http://www.emro.who.int/emrinfo/index.aspx?Ctry=pal, last updated: August
2010.
19. Palestinian Central Bureau of Statistics, 2009- Annual Report 2009. Palestine
ChildrenIssues and Statistics. Child Statistics Series (No. 12). Ramallah
Palestine. p33
20. Abdul Rahim H.F., Wick L., Halileh S.. et al., 2009- Maternal and child health in
the occupied Palestinian territory, The Lancet; 373(9667): 967-977
21. Garner S., Jarvis R., Emori G., et al., 1996- CDC definitions for nosocomial
infections. In: Olmsted R.N.: APIC Infection Control and Applied
Epidemiology: Principles and Practice, St. Louis: Mosby; USA, p: A1-A20.0
22. Wynn J., Cornell T., Wong H., et al., 2010- The Host Response to Sepsis and
Developmental Impact. Pediatr., 125(5):1031-1041.
23. Kaufman D. and Fairchild K., 2004- Clinical Microbiology of Bacterial and
Fungal Sepsis in Very Low Birth Weight Infants. Clin. Micr. Rev., 17(3): 638680.
24. Fanaroff A., Korones S., Wright L., et al., 1998- Incidence presenting features
risk factors and significance of late onset septicemia in very low birth weight
infants. NICHD Neo. Res. Net. Pediatr. Infect. Dis. J., 17:593-598.
25. Zaidi A.K., Thaver D., Ali S.A. and Khan T.A., 2009- Pathogens Associated
With Sepsis in Newborns and Young Infants in Developing Countries. Pediatr.
Infect. Dis. J.; 28 (1 Suppl): 1018.
79
26. Verani J.R., McGee L. and Schrag S.J.,, 2010- Prevention of perinatal Group B
Streptococcal disease revised guidelines from CDC. MMWR: 59 (RR-10): 1-23
27. Lowy F., 2003- Antimicrobial resistance the example of Staphylococcus aureus.
J. Clin. Inv., 111(9):1265-1273.
28. Klein E., Smith D. and Laxminarayan R., 2007- Hospitalizations and Deaths
Caused by Methicillin-Resistant Staphylococcus aureus United States19992005.
EID., 13(12):1840-1847.
29. Bialkowska- Hobrzanska H., Jaskot D. and Hammerberg O., 1993- Molecular
characterization of the coagulase-negative staphylococcal surface flora of
premature neonates. J. Gen. Micro., 139:2939-2944.
30. Toledano H., Schlesinger Y., Raveh D., et al., 2000- Prospective surveillance of
vancomycin resistant enterococci in a neonatal intensive care unit. Eur. J. Clin.
Micr., Infect. Dis., 19:282-287.
31. Stoll B.J., Hansen N., Fanaroff A., et al., 2002- Changes in pathogens causing
early onset sepsis in very low birth weight infants. N. Engl. J. Med., 347:240247.
32. Hanssler L., Rosenthal E. and Fitza B., 1990- Listeriosis in newborn infants.
Klin. Pad., 202(6):379-382.
33. Khan N., Wang Y., Kim K., et al., 2002- Cytotoxic necrotizing factor-1
contributes to Escherichia coli K1 invasion of the central nervous system. J. Biol.
Chem., 277:1560715612.
34. Sohn A.H., Garrett D.O., Sinkowitz-Cochran R.L., et al., 2001- Prevalence of
nosocomial infections in neonatal intensive care unit patients: results from the
first national point-prevalence survey. J. Pediatr. 139:821-827
35. Papasian C., Kinney J., Coffman S., et al., 1996- Transmission of Citrobacter
koseri from mother to infant documented by ribotyping and pulsed field gel
electrophoresis. Dia. Micr. Infect. Dis., 26:63-67.
36.
Goering R., Ehrenkranz N., Sanders C., et al., 1992- Long term epidemiological
analysis of Citrobacter diversus in a neonatal intensive care unit. Pediatr. Infect.
Dis. J., 11:99-104.
37. Carivaro V., Di Popolo A., Caprio A., et al., 2009- Pseudomonas aeruginosa in a
neonatal intensive care unit: molecular epidemiology and infection control
measures. BMC Infect.Dis., 9:70.
38. Moniri R., Mosayebi Z., Movahedian M., et al., 2006- Increasing Trend of
Antimicrobial Drug Resistance in Pseudomonas aeruginosa Causing Septicemia.
80
53. NNIS., 2004- National Nosocomial Infections Surveillance System Report, data
summary from January 1992 through June 2004. Am. J. Infect. Cont.; 32:470485.
54. Zaidi A.K., Huskins W.C., Thaver D., et al., 2005- Hospital-acquired neonatal
infections in developing countries. Lancet.; 365(9465): 1175-1188.
55. Bryce J., Boschi-Pinto C., Shibuya K., et al., 2005- WHO estimates of the causes
of death in children. Lanc., 365: 1147-1152.
56. Lawn J., Cousens S. and Zupan J., 2005- 4 million neonatal deaths: When?
Where? Why? Lancet,: 365: 891-900
57. Stoll B.J., 1997- The global impact of neonatal infection. Clin. Perinatol.;
24(1):1-21.
58. WHO,
2010-
World
Health
Statistics
2010:
66. Favier C., Vaughan E., De Vos W., et al., 2002- Molecular monitoring of
succession of bacterial communities in human neonates. Appl. Env. Micro.,
68:219-226.
67. Bennet R., Eriksson M. and Nord C., 2002- The fecal microflora of 13 month
old infants during treatment with eight oral antibiotics. Infec., 30(3):158-160.
68. Wall R., Ross R., Ryan C., et al., 2009- Role of gut microbiota in early infant
development. Cli. Med. Pediatr., 3 45-54.
69. Kerur B., Bhat B., Harish B., et al., 2006- Maternal genital bacteria and surface
colonization in early neonatal sepsis. Ind. J. Pediatr., 73:29-32.
70. CDC, 2000- Guidelines for preventing opportunistic infections among
hematopoietic stem cell transplant recipients. Recommendations of CDC, the
Infectious Disease Society of America, and the American Society of Blood and
Marrow Transplantation. MMWR, Morbidity & Mortality Weekly Report;
49(RR-10):1-125.
71. Bolyard E., Tablan O., Williams W., et al., 1998- Guideline for infection control
in healthcare personnel Hospital Infection Control Practices Advisory
Committee. Infect. Cont. Hosp. Epid., 19(6):407-463.
72. Rosen H., 1997- Acquisition of hepatitis C by a conjunctival splash. Am. J.
Infect. Cont., 25(3):242-7.
73. Beltrami E., Kozak A., Williams I., et al. 2003- Transmission of HIV and
hepatitis C virus from a nursing home patient to a health care worker. A. J.
Infect. Cont., 31(3):168-75.
74. Obasanjo O., Wu P., Conlon M., et al., 2001- An outbreak of scabies in a
teaching hospital lessons learned. Infect. Cont. Hosp. Epid., 22(1): 13-8.
75. Avitzur Y., Amir J., 2002- Herpetic whitlow infection in a general pediatrician
an occupational hazard. Infect.,30(4):234-6.
76. Duckro A., Blom D., Lyle E., et al., 2005- Transfer of vancomycin- resistant
enterococci via health care worker hands. Arch. Intern. Med., 165(3):302-7.
77. Berman D., Schaefler S., Simberkoff M. and Rahal J., 1986- Tourniquets and
nosocomial methicillin-resistant Staphylococcus aureus infections. N. Engl. J.
Med., 315:514-515.
78. Breathnach A., Jenkins D. and Pedler S., 1992- Stethoscopes as possible vectors
of infection by staphylococci. Br. Med. J., 305:1573-1574.
79. Brooks S., Khan A., Stoica D., et al., 1998- Reduction in vancomycin-resistant
Enterococcus and Clostridium difficile infections following change to tympanic
83
87. Srinivasan A., Wolfenden L., Song X., et al., 2003- An outbreak of Pseudomonas
aeruginosa infections associated with flexible bronchoscopes. N. Engl. J. Med.,
348(3):221-7.
88. Loh W., Ng V.V. and Holton J., 2000- Bacterial flora on the white coats of
medical students. .J. Hosp. Infect., 45:65-68.
89. Srinivasan A., Song X., Ross T., et al., 2002- A prospective study to determine
whether cover gowns in addition to gloves decrease nosocomial transmission of
vancomycin resistant enterococci in an intensive care unit. Infect. Cont. Hosp.
Epid., 23(8):424-8.
90. Piro S., Sammud M., Badi S. and Al Ssabi L., 2001- Hospital-acquired malaria
transmitted by contaminated gloves. J. Hosp. Infect., 47(2):156-8.
91. Korniewicz D., Kirwin M., Cresci K. and Larson E., 1993- Leakage of latex and
vinyl exam gloves in high and low risk clinical settings. Am. Ind. Hyg. Assoc. J.,
54(1):22-6.
92. Boyce J., Potter-Bynoe G., Chenevert C., King T., 1997- Environmental
contamination due to methicillin-resistant Staphylococcus aureus: possible
84
85
106. Cohen-Wolkowiez M., Moran C., Benjamin D., et al., 2009- Early and late
sepsis in late preterm infants. Pediatr. Infect. Dis. J., 28(12):1052-1056.
107. Lin F., Weisman L., Troendle J. and Adams K., 2003-Prematurity Is the Major
Risk Factor for Late-Onset Group B Streptococcus Disease. J. Infect. Dis.,
188(2), 267-271.
108. Mehall R., Kite A., Gilliam H., et al., 2002- Enteral feeding tubes are a reservoir
for nosocomial antibiotic resistant pathogens. J. Pediatr. Sur., 37:1011-1012.
109. OGrady N.P., Alexander M., Dellinger E.P., et al., 2002- Guidelines for the
Prevention of Intravascular Catheter-Related Infections. Infect. Control Hosp.
Epidemiol.; 23(12): 759-769
110. Haley R.W., Cushion N.B., Tenover F.C., et al., 1995- Eradication of endemic
methicillin-resistant Staphylococcus aureus infections from a neonatal intensive
care unit. J Infect Dis.;171(3):614-24.
111. Harbarth S., Sudre P., Dharan S., et al., 1999- Outbreak of Enterobacter cloacae
Related to Understaffing Overcrowding and Poor Hygiene Practices. Infect.
Cont. Hosp. Epid., 20(9): 598-603.
112. Profit J., Petersen L., McCormick M., et al., 2010- Patient to Nurse Ratios and
Outcomes of Moderately Preterm Infants. Pediatr., 125(2): 320-326.
113. Creedon S., 2005- Healthcare workers' hand decontamination practices:
compliance with recommended guidelines. J. Adv. Nurs., 51(3):208-216.
114. Albert R., and Condie F., 1981- Handwashing patterns in the medical intensive
care units. N. Engl. J. Med., 304:1465-6.
115. Doebbeling B., Stanley G., Sheetz C., et al., 1992- Comparative efficacy of
alternative hand washing agents in reducing nosocomial infections in intensive
care units. N. Engl. J. Med., 327:88-93.
116. Meengs M., Giles B., Chisholm C., et al., 1994- Hand washing frequency in an
emergency department. J. Em. Nur., 20:183-8.
117. Bischoff W., Reynolds T., Sessler C., et al., 2000- Handwashing compliance by
health care workers, the impact of introducing an accessible alcohol based hand
antiseptic. Arch. Intern. Med., 160:1017-21.
118. Pittet D. and Boyce J.M. 2001- Hand hygiene and patient care: Pursuing the
Semmelweis legacy. Lancet Infect. Dis.;1:9-20.
119. Saiman L., 2006- trategies for prevention of nosocomial sepsis in the neonatal
intensive care unit. Curr. Opin. Pediatr., 18(2):101-6.
120. Horan T. and Gaynes R., 2004- Surveillance of Nosocomial Infections, In:
86
Mayhall C.G., Hospital epidemiology and infection control. 3rd ed. Philadelphia:
Lippincott Williams & Wilkins; USA. p1659-1702
121. Tietjen L., Bossemeyer D. and McIntosh N., 2003- Infection Prevention
Guidelines for health care facilities with limited resources. United States
Agency for International Development, JHPIEGO Corporation, USA, p28-3.
122. Scheckler W., 1992- Continuous quality improvement in a hospital system
implications for hospital epidemiology. Infect. Cont. Hosp. Epid., 13:288-292.
123. Arya S., Agarwal N. and Agarwal S., 2008- Hospital acquired infection point
prevalence or culture-based surveillance?. Brit. J. Infect. Cont., 9(2):23-24.
124. Haas J. and Trezza A., 2002- Outbreak investigation in a neonatal intensive care
unit. Sem. Per., 26:367-378.
125. Gastmeier P., Loui A., Stamm-Balderjahn S., et al., 2007- Outbreaks in neonatal
intensive care units - they are not like others. Am J Infect Control.;35(3):172-6.
126. Decembrino L., Perrini S. and Stronati M., 2010- Surveillance of infection events
in neonatal intensive care. Minerva Pediatr.;62(3 Suppl 1):41-45.
127. Stratton W., and Greene N., 2004- Role of the Microbiology Laboratory in
Hospital Epidemiology and Infection Control: In: Mayhall CG, editor.
Hospital epidemiology and infection control. 3rd ed. Philadelphia: Lippincott
Williams & Wilkins, USA, p1809-1825
128. Siegel J., Rhinehart E., Jackson M., et al., 2007- 2007 Guideline for Isolation
Precautions: Preventing Transmission of Infectious Agents in Healthcare
Settings. Am. J. Infect. Control; 35(10 Suppl 2):S65-164.
129. Grschel D., 1980- Air sampling in hospitals. Ann. N.Y. Acad. Sci., 353: 23040.
130. Barbaree J., Gorman G., Martin B.S., et al., 1987- Protocol for sampling
environmental sites for Legionellae. Appl. Env. Micro., 53:1454-8.
131. McGowan J.E.. .Jr, and Weinstein R.A., 1998- The role of the laboratory in
control of nosocomial infection. In: Bennett J.V., Brachman P.S., Hospital
infections, 4th ed., PA: Lippincott Raven, USA, p14364.
132. Sehulster L., Chinn R., Arduino M., et al., 2004- Guidelines for environmental
infection control in health-care facilities. Recommendations from CDC and the
Healthcare Infection Control Practices Advisory Committee (HICPAC). Chicago
IL; American Society for Healthcare Engineering/American Hospital
Association;.
133. Gerberding J., 1998- Nosocomial transmission of opportunistic infections. Infect.
Cont. Hosp. Epid., 19:574-7.
87
134. Maki D., Alvarado C., Hassemer C. and Zilz M., 1982- Relation of the inanimate
hospital environment to endemic nosocomial infection. N. Engl. J. Med.,
307:1562-6.
135. Spaulding E., 1972- Chemical disinfection and antisepsis in the hospital. J. Hosp.
Res., 9:5-31.
136. Rutala W., Weber D., and the Healthcare Infection Control Practices Advisory
Committee (HICPAC), 2008- Guideline for Disinfection and Sterilization in
Healthcare Facilities, CDC, USA
137. Bhattachatyya M. and Kepnes L., 2004- The effectiveness of immersion
disinfection for flexible fiberoptic laryngoscopes. Oto. H. N., 130:681-5.
138. Hamasuna R., Nose K., Sueyoshi T., et al., 2004- High level disinfection of
cystoscopic equipment with ortho phthalaldehyde solution. J. Hosp. Infect.,
57:346-8.
139. Sehulster L. and Chinn R., 2003- Healthcare Infection Control Practices
Advisory Committee. Guidelines for environmental infection control in health
care facilities. MMWR, 52:1-44.
140. Bhalla A., Pultz N., Gries D., et al. 2004- Acquisition of nosocomial pathogens
on hands after contact with environmental surfaces near hospitalized patients.
Infect. Cont. Hosp. Epid., 25:164-7.
141. Westwood J., Mitchell M. and Legace S., 1971- Hospital sanitation the massive
bacterial contamination of the wet mop. Appl. Micr., 21:693-697.
142. Gerdes J., 2004- Diagnosis and management of bacterial infections in the
neonate. Pediatr. Clin. Nor. Am., 51:939-959.
143. Vergnano S., Sharland M., Kazembe P., et al., 2005 Neonatal sepsis an
international perspective. Arch. Dis. Child. Fet. Neo. Ed., 90(3): F220-F224.
144. Paul M., Schlesinger A., Grozinsky-Glasberg S., et al., 2003- Beta-lactam versus
Beta-lactam-aminoglycoside combination therapy in cancer patients with
neutropaenia. Cochrane Database of Systematic Reviews; Issue 3. Art. No.:
CD003038. http://www2.cochrane.org/reviews/en/ab003038.html accessed: June
16. 2011
145. Levin B. and Bonten M., 2004- Cycling antibiotics may not be good for your
health. PNAS., 101(36):13101-13102.
146. WHO, 2001- WHO Global strategy for containment of antimicrobial
resistance, WHO, Switzerland, p1
147. Mulvey M. and Simor A., 2009- Antimicrobial resistance in hospitals: How
concerned should we be?. Can. Med. Ass. J., 180(4):408-415.
88
148. Toltzis P., 2003- Colonization with antibiotic resistant Gram negative bacilli in
the neonatal intensive care unit. Min. Pediatr., 55(5):385-93.
149. Davies J. and Davies D., 2010- Origins and Evolution of Antibiotic Resistance.
Micro. Mol. Bio. Rev., 74(3):417-33.
150. Lipsitch M. and Samore M., 2002- Antimicrobial use and antimicrobial
resistance: a population perspective. EID., 8:347-54.
151. Kenyon S., Taylor D. and Tarnow-Mordi W., 2001- ORACLE Collaborative
Group. Broad-spectrum antibiotics for preterm prelabour rupture of fetal
membranes: the ORACLE I randomised trial. Lan., 357:979-88.
152. Jones R., 2001- Resistance patterns among nosocomial pathogens trends over the
past few years. Chest., 119(2 Suppl):397S-404S.
153. Isaacs D., 2006- Unnatural selection: reducing antibiotic resistance in neonatal
units. Arch. Dis. Chil. Fet. Neo., 91(1): F72F74.
154. Archibald L.K. and Reller L.B., 2001- Clinical microbiology in developing
countries. Emerg. Infect. Dis.;7:302-305.
155. Masterton R., 2005- Antibiotic cycling more than it might seem. J. Anti. Chem.,
55(1):1-5.
156. Brown E. and Nathwani D., 2005- Antibiotic cycling or rotation: a systematic
review of the evidence of efficacy. J. Anti. Chem., 55(1): 6-9.
157. Wang Y. and Lipsitch M., 2006- Upgrading antibiotic use within a class
Tradeoff between resistance and treatment success. PNAS., 103(25): 9655-9660.
158. Toltzis P., Dul M., Hoyen C., et al., 2002- The Effect of Antibiotic Rotation on
Colonization With Antibiotic Resistant Bacilli in a Neonatal Intensive Care Unit.
Pediatr., 110(4): 707 -711.
159. Bergstrom C., Lo M. and Lipsitch M., 2004- Ecological theory suggests that
antimicrobial cycling will not reduce antimicrobial resistance in hospitals.
PNAS., 101(36): 13285-13290.
160. Drew R., 2009- Antimicrobial Stewardship Programs: How to Start and Steer a
Successful Program. J. Man. Care Pharm., 15(2)(Suppl):S18-S23.
161. Fisherman N., 2006- Antimicrobial stewardship. Am. J. Med., 119 (6 Suppl1):
S53-S70.
162. Lautenbach E. and Polk R., 2007- Resistant gram-negative bacilli: A neglected
healthcare crisis? Am. J. Heal.-Sys. Phar., 64(23) Supp. 14: S3-S21.
89
163. Kollef M., 2006- Is Antibiotic Cycling the Answer to Preventing the Emergence
of Bacterial Resistance in the Intensive Care Unit? Clin. Infect. Dis., 43 (Supp.
2) S82-S88.
164. Tagare A., Kadam S., Vaidya U. and Pandit A., 2009- Routine antibiotic use in
preterm neonates: a randomised controlled trial. J. Hosp. Infect., 74(4):332-336.
165. Deresinski S., 2007- Principles of Antibiotic Therapy in Severe Infections:
Optimizing the Therapeutic Approach by Use of Laboratory and Clinical Data.
Clin. Infect. Dis., 45 (Supp. 3): S177-S183 .
166. Schramm G., Johnson J., Doherty J., et al., 2006- Methicillin resistant
Staphylococcus aureus sterile site infection the importance of appropriate initial
antimicrobial treatment. Crit. Care Med., 34:2069-2074.
167. Franz A., Steinbach G., Kron M. and Pohlandt F., 1999- Reduction of
Unnecessary Antibiotic Therapy in Newborn Infants Using Interleukin-8 and CReactive Protein as Markers of Bacterial Infections. Pediatr., 104(3):447 -453.
168. MacDougall C. and Polk R., 2005- Antimicrobial Stewardship Programs in
Health Care Systems. Clin. Micr. Rev., 18(4):638-656.
169. Wilson M.L., Mitchell M., Morris A.J., et al., 2007- Principles and producers
for blood culture; approved guidelines. CLSI, USA, P:7-10.
170. Angelotti R., Foter M., Busch K. and Lewis K., 1958- A comparative evaluation
of methods for determining the bacterial contamination of surfaces. Food
Research; 23:17585.
171. Campf G. and Ostermeyer C., 2005- Efficacy of two distinct ethanol-based hand
rubs for surgical hand disinfection a controlled trial according to prEN 1279.
BMC Infect. Dis., 5:17.
172. Pechorsky A., Nitzan Y. and Lazarovitch T., 2009- Identification of pathogenic
bacteria in blood cultures: Comparison between conventional and PCR methods.
J. Micr. Meth., 78(3): 325-330.
173. Wikler M., Cockerill F., Bush K., et al., 2009 - Performance Standards for
Antimicrobial Disk Susceptibility Tests.10th ed., CLSI, USA, P:8-12.
174. Griffin M. and Moorman J., 2001- Toward the early diagnosis of neonatal sepsis
and sepsis like illness using novel heart rate analysis. Pediatr., 107(1):97-104.
175. El Jadba A., El Yazji M., 2009- Neonatal septicemia in Gaza City hospitals. Pak.
J. Med. Sci., 25(2): 226-231.
176. Greenberg D., Shinwell E., Yagupsky P., et al., 1997- A prospective study of
neonatal sepsis and meningitis in southern "Israel". Pediatr. Infect. Dis. J.,
16(8):768-73.
90
177. Bromiker R., Arad I., Peleg O., et al., 2001- Neonatal bacteremia: patterns of
antibiotic resistance. Infect. Cont. Hosp. Epid., 22(12):767-70.
178. Watson R., Carcillo J., Linde Z., et al., 2003- The Epidemiology of Severe Sepsis
in Children in the United States. Am. J. Res. Cri. Care Med., 167: 695-701.
179. Chen L., Sexton D., Kaye K. and Anderson D., 2009- Patient-days: A better
measure of incidence of occupational blood borne exposures. A.J. Infec. Con.,
37(7): 534-540.
180. Makhoul I., Sujov P., Smolkin T., et al., 2002- Epidemiological clinical and
microbiological characteristics of late onset sepsis among very low birth weight
infants in "Israel" a national survey. Pediatr., 109(1):34-39.
181. Karpuch J., Goldberg M., Kohelet D., 1983- Neonatal bacteremia. A 4-year
prospective study. Isr. J. Med. Sci., 19(11):963-966.
182. Haley R., and Bregman D., 1982- The role of understaffing and overcrowding in
recurrent outbreaks of Staphylococcal infections in a neonatal intensive care
unit. J. Infect. Dis., 145(6): 875-885.
183. Grauel E., Halle E., Bollmann R., et al., 1989- Neonatal Septicaemia Incidence,
Etiology and Outcome A 6-year Analysis. Acta. Pediatr.; 78 (s360): 113-119.
184. Dimick J., Swoboda S., Provonost P., et al., 2001- Effect of nurse-to-patient ratio
in the intensive care unit on pulmonary complications and resource use after
hepatectomy. Am. J. Crit. Care, 10:(6):376-382.
185. Andersen B., Lindemann R., Bergh K., et al., 2002- Spread of methicillinresistant Staphylococcus aureus in a neonatal intensive-care unit associated with
understaffing overcrowding and mixing of patients. Hosp. Infect.,50(1):18-24.
186. Stegenga J., Bell E., Matlow A., 2002- The role of nurse understaffing in
nosocomial viral gastrointestinal infections on a general pediatrics ward. Infect.
Cont. Hosp. Epid., 23 (3):133-6.
187. Parry G., 2005- Relationship between probable nosocomial bacteraemia and
organisational and structural factors in UK neonatal intensive care units. Qual.
Saf. Heal. Care., 14:264-269.
188. Beggs C., Noakes C., Shepherd S., et al., 2006- The influence of nurse cohorting
on hand hygiene effectiveness. A. J. Infect. Cont., 34(10): 621-626.
189. Cimiotti J., Haas J., Saiman L. and Larson E., 2006- Impact of Staffing on
Bloodstream Infections in the Neonatal Intensive Care Unit. Arch. Pediatr. Ado.
Med., 160:832-836.
190. Clements A., Halton K., Graves N., et al., 2008- Overcrowding and understaffing
in modern health-care systems: key determinants in methicillin-resistant
91
92
203. Marra A., Guastelli L., de Arajo C., et al., 2011- Positive deviance: a program
for sustained improvement in hand hygiene compliance. Am. J. Infect. Cont.,
39(1):1-5.
204. Creedon S., Slevin B., De Souza V., et al., 2008- Hand hygiene compliance:
exploring variations in practice between hospitals. Nurs. T., 104 (49): 32-35.
205. Gould D.J., Moralejo D., Drey N. and Chudleigh J.H.. 2010- Interventions to
improve hand hygiene compliance in patient care. Cochrane Database of
Systematic
Reviews,
Issue
9.
Art.
No.:
CD005186,
DOI:
10.1002/14651858.CD005186.pub3
206. Lankford M., Zembower T., Trick W., et al., 2003- Influence of Role Models and
Hospital Design on Hand Hygiene of Healthcare Workers. EID., 9(2):217-223.
207. O'Connell N. and Humphreys H., 2000- Intensive care unit design and
environmental factors in the acquisition of infection. J. Hosp. Infect., 45(4): 255262.
208. Hibbard J., 2004- New Roles for Patients and Consumers in Assuring High
Quality Care. Vir. Men., 6(6).
209. Javetz R. and Stern Z., 1996- Patients complaints as a management tool for
continuous quality improvement. J. Mng. Med., 10(3): 39-48.
210. Hibbard J., Stockard J. and Tusler M., 2003- Does publicizing hospital
performance stimulate quality improvement efforts? Heal. Aff., 22:84-94.
211. Trigg L., 2011- Patients' opinions of health care providers for supporting choice
and quality improvement. J. Heal. Ser. Res. & Poli., 16:102.
212. Schwappach, D., 2010- Engaging patients as vigilant partners in safety. Med.
Care Res. Rev., 67(2): 119-148.
213. Longtin Y., Sax H., Leape L., et al., 2010- Patient participation Current
knowledge and applicability to patient safety. Mayo. Clin. Proc., 85(1): 53-62.
214. Boyce J., 2007- Environmental contamination makes an important contribution
to hospital infection. J. Hosp. infect., 35:50-54.
215. Byers K., Durbin L., Simonton B., et al., 1998- Disinfection of hospital rooms
contaminated with vancomycin-resistant Enterococcus faecium. Infect. Cont.
Hosp. Epid., 19(4): 261-264.
216. Martinez J., Ruthazer R., Hansjosten K., et al., 2003- Role of environmental
contamination as a risk factor for acquisition of vancomycin resistant
enterococci in patients treated in a medical intensive care unit. Arch. Inter. Med.,
163:1905-1912.
93
217. French G., Otter J., Shannon K., et al., 2004- Tackling contamination of the
hospital environment by methicillin-resistant Staphylococcus aureus (MRSA): a
comparison between conventional terminal cleaning and hydrogen peroxide
vapour decontamination. J. Hosp. Infect., 57:31-37.
218. Cooper R., Griffith C., Malik R., et al., 2007- Monitoring the effectiveness of
cleaning in four British hospitals. A. J. Infect. Cont., 35(5):338-341.
219. CDC, 1999- National Institute for Occupational Safety and Health. NIOSH Alert:
Preventing needle stick injuries in health care settings. NIOSH Publication No.
2000-108. http://www.cdc.gov/niosh/docs/2000-108/ accessed: May 15, 2011
220. Flores A. and Pevalin D., 2006- Healthcare workers' compliance with glove use
and the effect of glove use on hand hygiene compliance. J. Infect. Prev., 7(6): 1519.
221. Haas J. and Larson E., 2008- Compliance with Hand Hygiene Guidelines: Where
are we in 2008?. Am. J. Nur., 108(8): 40 - 44.
222. Asare A., Enweronu-Laryea C. and Newman M., 2009- Hand hygiene practices
in a neonatal intensive care unit in Ghana. J. Infect. Dev. Count., 3: 352-356.
223. WHO, 2005- WHO Guidelines on Hand Hygiene in Health Care (Advanced
Draft): A Summary: http://www.who.int/patientsafety/events/05/HH_en.pdf.
accessed: May 15, 2011
224. Sax H., Allegranzi B., Chrati M., et al., 2009- The World Health Organization
hand hygiene observation method. Am. J. Infect. Cont., 37:827-34.
225. Garner S. and Favero M., 1985- CDC guideline for handwashing and hospital
environmental control. Infect. Cont., 7:231-43.
226. Larson E., 1995- APIC guideline for handwashing and hand antisepsis in health
care settings. Am. J. Infect. Cont., 23:251-69.
227. CDC, 2002- Guideline for Hand Hygiene in Health Care Settings
Recommendations of the Healthcare Infection Control Practices Advisory
Committee and the HICPAC/SHEA/APIC/IDSA Hand Hygiene Task Force.
MMWR, 51(No. RR- 16).
228. Ehrenkranz N., and Alfonso B., 1991- Failure of bland soap handwash to
prevent hand transfer of patient bacteria to urethral catheters. Infect. Cont.
Hosp. Epid., 12(11):654-62.
229. Allegranzi B., and Pittet D., 2009- Role of hand hygiene in health careassociated infection prevention. J. Hosp. Infect., 73: 305-315.
94
230. Allegranzi B., Sax H., Bengaly L., et al., 2010- World Health Organization
"Point G" Project Management Committee Successful implementation of the
World Health Organization hand hygiene improvement strategy in a referral
hospital in Mali, Africa. Infect. Cont. Hosp. Epid., 31(2):133-41.
231. Nthumba P., Stepita-Poenaru E., Poenaru D., et al., 2010- Cluster randomized
crossover trial of the efficacy of plain soap and water versus alcohol based rub
for surgical hand preparation in a rural hospital in Kenya. Bri. J. Sur.,
97(11):1621-1628.
232. Rosenthal V., Guzman S. and Safdar N., 2005- Reduction in nosocomial infection
with improved hand hygiene in intensive care units of a tertiary care hospital in
Argentina. Am. J. Infect. Cont., 33: 392-97.
233. Damani N., 2007- Simple measures save lives: An approach to infection control
in countries with limited resources. J. Hosp. Infect., 65(suppl.2): 151-54.
234. Le T., Dibley M., Vo V., Archibald L., et al., 2007- Reduction in surgical site
infections in neurosurgical patients associated with a bedside hand hygiene
program in Vietnam. Infect. Cont. Hosp. Epid., 28: 583-88.
235. Kramer A., Schwebke I. and Kampf G., 2006- How long do nosocomial
pathogens persist on inanimate surfaces? A systematic review. BMC Infect. Dis.,
6:130.
236. Harris A., 2008- How Important Is the Environment in the Emergence of
Nosocomial Antimicrobial Resistant Bacteria?. Clin. Infect. Dis., 46(5): 686688.
237. Huang S., Datta R. and Platt R., 2006- Risk of Acquiring Antibiotic Resistant
Bacteria From Prior Room Occupants. Arch. Intern. Med.,166:1945-1951.
238. Drees M., Snydman D., Schmid C., et al., 2008- Prior Environmental
Contamination Increases the Risk of Acquisition of Vancomycin-Resistant
Enterococci. Clin.Infect. Dise., 46:678-685.
239. Wenzel R.P., 1994- Healthcare workers and the incidence of nosocomial
infection: can treatment of one influence the other?--a brief review. J Chemother.
Suppl 4:33-37.
240. Gupta V., Bhoi S., Goel A. and Admane S., 2008- Nosocomial dengue in health
care workers. Lan., 371(9609): 299.
241. Komitova R., Kunchev A., Mihneva Z. and Marinova L., 2011- Nosocomial
transmission of measles among healthcare worker Bulgaria 2010.
Eurosurveillance;16(15): 1-3
95
242. Cassillas A., Nyamathi A., Sosa A., et al., 2003- review of Ebola virus:
pathogenesis, clinical presentation, and diagnostic assessment. Biol. Res. Nurs.,
4:268-275.
243. Moore G. and Griffith C., 2007- Problems associated with traditional hygiene
swabbing the need for in house standardization. J. Appl. Micr., 103(4):1090-103.
244. Landers T.F., Hoet A. and Wittum T.E., 2010- Swab type, moistening, and
preenrichment for Staphylococcus aureus on environmental surfaces. J Clin
Microbiol.;48(6):2235-6.
245. Bugajny A., Knopkiewicz M., Piotraszewska-Pajk A., et al., 2005- On the
Microbiological Quality of the Outdoor Air in Pozna, Poland. P. J. Env. St.,
14(3): 287-293.
246. Oyetayo P. and Ilori R., 2007- Microbial quality and antibiotic sensitivity
patterns of bacterial isolated from different sections of a state specialist hospital.
Res. J. Micr., 2(5): 496-499.
247. Kaur N. and Hans C., 2007- Air bacterial isolations from operation theatres in a
tertiary care hospital in India.. J. Clin. Diag. Res., 1(2):87-89.
248. Stryjakowska-Sekulska M., Piotraszewska-Pajk A., Nowicki M. and Filipiak
M., 2007- Microbiological Quality of Indoor Air in University Rooms. Pol. J.
Env. Stud., 16(4): 623-632.
249. Ekhaise F., Ighosewe O. and Ajakpovi O., 2008- Hospital Indoor Airborne
Microflora in Private and Government Owned Hospitals in Benin City, Nigeria.
W. Afr. J. Med. Sci., 3 (1): 19-23.
250. Dahran S. and Pittet D., 2002- Environmental controls in operating theaters. J.
Hosp. Infect., 51: 79-84.
251. Federal Standard 209E. 1992- Airborne particulate cleanliness classes in clean
rooms and clean zones. United States General Service Administration.
http://www.set3.com/papers/209e.pdf. accessed: May 6, 2011
252. Charles K., Magee R., Won D., and Lusztyk E., 2005- Indoor Air Quality
Guidelines and Standards. National Research Council Canada, RR-204.
253. The Government of the Hong Kong Special Administrative Region., 2003- A
Guide
on
Indoor
Air
Quality
Certification
Scheme.
http://www.iaq.gov.hk/cert/doc/CertGuide-eng.pdf. accessed: May 12- 2011
254. Updegraff D., 1964- A cultural method of quantitatively studying the
microorganisms on the skin. J. Inv. Der., 43:129-137.
255. Williamson P. and Kligman A., 1965- A new method for the quantitative
96
97
268. Newman M., 2002- Neonatal intensive care units: Reservoirs of nosocomial
pathogens. W. Afr. J. Med., 21(4): 310-312.
269. Bykyavuz B., Adiloglu A., Onal S., et al., 2006- Finding the sources of
septicemia at a neonatal intensive care unit: newborns and infants can be
contaminated while being fed. Jpn. J. Infect. Dis., 59(4):213-5.
270. Adler A., Gottesman G., Dolfin T., et al., 2005- Bacillus species sepsis in the
neonatal intensive care unit. J Infect., 51(5):390-395.
271. Cruz A., Cazacu A. and Allen C., 2007- Pantoea agglomerans, a Plant Pathogen
Causing Human Disease. J. Clin. Micro., 45(6): 1989-92.
272. Habsah H., Zeehaida H., Van Rostenberghe R., et al., 2005- An outbreak of
Pantoea spp. in a neonatal intensive care unit secondary to contaminated
parenteral nutrition. J. Hosp. Infect., 61:213-218.
273. Sirinavin S., Likitnukul S. and Lolekha S., 1984- Aeromonas septicemia in
infants and children. Pediatr. Infect. Dis., 3(2):122-5.
274. Watterson J., Williams P. and Durbin R., 1971- Response of cucurbits to Erwinia
tracheiphila. Pla. Dis. Rep., 55:816-819.
275. Bottone E. and Schneierson S., 1972- Erwinia species: an emerging human
pathogen. Am. J. Clin. Pathol., 57(3):400-405.
276. Meyers B., Bottone E., Hirschman S. and Schneierson S. 1972- Infections
Caused by Microorganisms of the Genus Erwinia. Ann. Int. Med., 76(1): 9-14.
277. Levinson D., 1983- Information, computers, and clinical practice. JAMA; 249:
607-609.
278. McDonald C. and Tierney W., 1988- Computer stored medical records their
future role in medical practice. JAMA., 259:3433-3440.
279. Greenes R. and Shortliffe E., 1990- Medical informatics: an emerging academic
discipline and institutional priority. JAMA, 263:1114-1120.
280. Morgan J., 1992- The electronic health record challenges the health information
management profession. J. AHIMA., 63:79-85.
281. Winslow E.H., Nestor V.A., Davidoff S.K., et al., 1997- Legibility and
completeness of physicians' handwritten medication orders. Heart
Lung.;26(2):158-64.
282. Tettelbach W.H. and Classen D.C. 2004- The Electronic Health Record: An
Essential Technology for Hospital Epidemiology. In: Mayhall CG, editor.
Hospital epidemiology and infection control. 3rd ed. Philadelphia: Lippincott
Williams & Wilkins, USA,p207-228.
98
283. Cannon J. and Pierre B., 1997- Gender differences in host defense mechanisms.
J. Psy. Res., 31(1):99-113.
284. Spitzer J., 1999- Gender differences in some host defense mechanisms. Lup.,
8(5):380-3.
285. Da Silva J., 1999- Sex hormones and glucocorticoids: interactions with the
immune system. Ann. N. Y. Acad. Sci., 876:102-17.
286. Caruso R., Bellocco R., Pagano M., et al., 2002- Prognostic Value of
Intratumoral Neutrophils in Advanced Gastric Carcinoma in a High-Risk Area in
Northern Italy. M. D. Mod. Pathol., 15(8):831-837.
287. Hebert P., Reed G., Entman S., et al., 1999- Serious maternal morbidity after
childbirth prolonged hospital stays and readmissions. Obs. Gyn., Dec.,
94(6):942-7.
288. Kuzma J., 2008- Randomized clinical trial to compare the length of hospital stay
and morbidity for early feeding with opioid sparing analgesia versus traditional
care after open appendectomy. Clin. Nutr., 27(5): 694-699.
289. rtenstrand A., Westrup B., Brostrm E., et al., 2010 - The Stockholm Neonatal
Family Centered Care Study: Effects on Length of Stay and Infant Morbidity.
Pediatr. 125(2): e278 -e285.
290. Jaggers J., Harrison J., Bashore T., et al., 1998- The Ross procedure: shorter
hospital stay, decreased morbidity, and cost effective. Ann. Thor. Surg.,
65(6):1553-7.
291. Davies K., Bell T., Miller J., et al., 2011- Hospital Costs, Length of Stay and
Mortality Associated with Childhood, Adolescent and Young Adult
Meningococcal Disease in the US. Appl. Heal. Econ. Heal. Poli., 9(3): 197-207.
292. Wong E., Cheung A., Leung M., et al., 2011- Unplanned readmission rates,
length of hospital stay, mortality, and medical costs of ten common medical
conditions: a retrospective analysis of Hong Kong hospital data. BMC, 11:149
293. Rostenberghe H., 2009- Bacteriology of early versus late onset neonatal sepsis. J.
Pediatr. Infect. Dis., 4(3): 197-198.
294. Fernando A., Heath P. and Menson E., 2008- Antimicrobial policies in the
neonatal units of the United Kingdom and Republic of Ireland. J. Anti. Chem.,
61: 743-745.
295. Lemons J., Bauer C., Oh W., et al., 2001- Very low birth weight outcomes of the
National Institute of Child health and human development neonatal research
network, January 1995 through December 1996. Pediatr., 107(1):E1.
99
296. Lasswell S., Barfield W., Rochat R. and Blackmon L., 2010- Perinatal
regionalization for very low-birth-weight and very preterm infants: a metaanalysis. JAMA., 304(9):992-1000.
297. Murphy D., Liebling R., Verity L., et al., 2001- Maternal and neonatal morbidity
associated with operative delivery in second stage of labour. Lan.,
358(9289):1203-1207.
298. Hernndez-Daz S., Van Marter L., Werler M., et al., 2007- Risk Factors for
Persistent Pulmonary Hypertension of the Newborn. Pediatr. 120(2): e272 -e282.
299. De Luca R., Boulvain M., Irion O., et al., 2009- Incidence of Early Neonatal
Mortality and Morbidity After Late-Preterm and Term Cesarean Delivery.
Pediatr.; 123(6): e1064 -e1071.
300. Liston F., Allen V., OConnell V., and Jangaard K., 2008- Neonatal outcomes
with caesarean delivery at term. Arch. Dis. Chil. Fet. Neo. Ed., 93:F176-F182.
301. McLaren R., Chauhan S. and Gross T., 1996- Intrapartum factors in early onset
group B streptococcal sepsis in term neonates: A case-control study. Am. J. Obs.
Gyn., 174(6): 1934-1940.
302. Hook B., Kiwi R., Amini S., et al., 1997- Neonatal Morbidity After Elective
Repeat Cesarean Section and Trial of Labor. Pediatr., 100(3): 348-353.
303. Veronesi M., Panzani S., Faustini M. and Rota A., 2009- An Apgar scoring
system for routine assessment of newborn puppy viability and short term survival
prognosis. Ther., 72: 401-407.
304. Weinberger B., Anwar M., Hegyi T., et al., 2000- Antecedents and Neonatal
Consequences of Low Apgar Scores in Preterm Newborns A Population Study.
Arch. Pediatr. Ado. Med., 154:294-300.
305. Moster D., Lie R. and Markestad T., 2002- Joint association of Apgar scores and
early neonatal symptoms with minor disabilities at school age. Arch. Dis. Child.
Fet.Neo. Ed., 86:F16-F21.
306. Soman M., Green B. and Daling J., 1985- Risk factors for early neonatal sepsis.
Am. J. Epid., 121 (5): 712-719.
307. Shah G.S., Budhathoki S., Das B.K. and Mandal R.N. 2006- Risk factors in early
neonatal sepsis. Kathmandu Univ. Med. J.; 4-2 (14): 187-191
308. WHO, 2000- Management of the child with serious infection or severe
malnutrition: guidelines for care at the first-referral level in developing
countries. Department of Child and Adolescent Health and Development.
Geneva: WHO: p74-79.
100
309. Kayser F., Morenzoni G., Strssle A. and Hadorn K., 1989- Activity of
meropenem against gram positive bacteria. J. Anti. Chem.,24 Suppl A:101-112.
310. Hellinger W. and Brewer N., 1999- Carbapenems and monobactams imipenem
meropenem and aztreonam. Mayo. Clin. Proc., 74(4):420-434.
311. Joly-Guillou M., Kempf M., Cavallo J., et al., 2010- Comparative in vitro activity
of Meropenem Imipenem and Piperacillin/tazobactam against 1071 clinical
isolates using 2 different methods: a French multicentre study. BMC. Infect.
Dis., 10:72-81.
312. Goto K., Ohi T., Namba A., et al., 2011-Successful Treatment of Methicillin
resistant Staphylococcus aureus Meningitis by Intrathecal Injection of
Vancomycin. Shinkei kenkyu no shinpo (Brain and nerve).; 63(4):417-421.
313. Steward C., Mohammed J., Swenson J., et al., 2003- Antimicrobial susceptibility
testing of carbapenems multicenter validity testing and accuracy levels of five
antimicrobial test methods for detecting resistance in Enterobacteriaceae and
Pseudomonas aeruginosa isolates. J. Clin. Micr., 41(1):351-358.
314. Babay H., Manneh K. and Somily A., 2009- Accuracy of Detecting Resistance to
Carbapenems among Gram Negative Rods Comparison of Three Methods. J. o T.
Univ. Med. Scie., 4(1): 53-61.
315. Tenover F., Kals R., Williams P., et al., 2006- Carbapenem Resistance in
Klebsiella pneumoniae Not Detected by Automated Susceptibility Testing. E.I.D.,
12(8):1209-1213.
316. Chaudhary U., Aggarwal R., 2004- Extended spectrum -lactamases - An
emerging threat to clinical therapeutics. Ind. J. Med. Micr., 22:75-80.
317. Ben-Ami R., Rodrguez-Bao J., Arslan H., et al. 2009- A multinational survey of
risk factors for infection with extended spectrum beta lactamase producing
enterobacteriaceae in nonhospitalized patients. Clin. Infect. Dis., 49(5):682-690.
318. Tzelepi E., Giakkoupi P., Sofianou D., et al., 2000- Detection of Extended
Spectrum Lactamases in Clinical Isolates of Enterobacter cloacae and
Enterobacter aerogenes. J. Clin. Micr., 38(2): 542-546.
319. Bradford P., 2001- Extended-spectrum beta-lactamases in the 21st century:
characterization, epidemiology, and detection of this important resistance threat.
Clin. Micro. Rev., 14(4):933-51.
320. Borer A., Gilad J., Menashe G., et al., 2002- Extended spectrum beta lactamase
producing Enterobacteriaceae strains in community acquired bacteremia in
southern "Israel". Med. Sci. Monit., 8:CR44-47.
101
321. Karsh T., Tawfik A., Al-Shammary F., et al., 1995- Antimicrobial resistance and
prevalence of extended spectrum beta lactamase among clinical isolates of gram
negative bacteria in Riyadh. J. Chem., 7:509-514.
322. Barguellil F., Burucoa C., Amor A., et al., 1995- In vivo acquisition of extended
spectrum beta lactamase in Salmonella enteritidis during antimicrobial therapy.
Eur. J. Clin. Micro. Infect. Dis., 14:703-706.
323. Mhand R., Brahimi N., Moustaoui N., et al., 1999- Characterization of extended
spectrum beta-lactamase-producing Salmonella typhimurium by phenotypic and
genotypic typing methods. J. Clin. Micr., 37:3769-3773.
324. Astal Z., Sharif F., Abdallah S., Fahd M., 2004- Extended spectrum betalactamases in Escherichia coli isolated from community acquired urinary tract
infections in the Gaza Strip, Palestine. Ann. Saudi Med., 24(1): 55-57.
325. Paterson D., Ko W., Von Gottberg A, et al., 2004- Antibiotic therapy for
Klebsiella pneumoniae bacteremia implications of production of extendedspectrum beta-lactamases. Clin. Infect. Dis., 39(1):31-37.
326. Mody R., Erwin D., Summers A., et al,. 2007- Ertapenem susceptibility of
extended spectrum beta-lactamase-producing organisms. Ann. Clin. Micr. Anti.
6:6-11.
327. Garau J., 2008- Other antimicrobials of interest in the era of extended-spectrum
beta-lactamases: fosfomycin, nitrofurantoin and tigecycline. Clin. Micr. Infect.,
14 Suppl 1:198-202.
328. Cantn R. and Coque T., 2006- The CTX-M beta-lactamase pandemic.Curr.
Opin. Micr., 9(5):466-475.
329. Zimhony O., Chmelnitsky I., Bardenstein R., et al., 2006- Endocarditis caused by
extended spectrum beta lactamase producing Klebsiella pneumoniae emergence
of resistance to ciprofloxacin and piperacillin tazobactam during treatment
despite initial susceptibility. Anti. Agen. Chem., 50(9):3179-3182.
330. Deguchi T., Fukuoka A., Yasuda M., et al., 1997- Alterations in the GyrA subunit
of DNA gyrase and the ParC subunit of topoisomerase IV in quinolones resistant
clinical isolates of Klebsiella pneumoniae. Anti. Agen. Chem., 41:699-701.
331. Bagel S., Hullen V., Wiedemann B. and Heisig P., 1999- Impact of gyrA and
parC mutations on quinolone resistance, doubling time, and supercoiling degree
of Escherichia coli. Anti. Agen. Chem., 43:868-75.
332. Paterson D., Mulazimoglu L., Casellas J., et al., 2000- Epidemiology of
Ciprofloxacin Resistance and Its Relationship to Extended Spectrum bLactamase Production in Klebsiella pneumoniae Isolates Causing Bacteremia.
Clin. Infect. Dis., 30:473-478.
102
333. Livermore D., James D., Reacher M., et al., 2002- Trends in Fluoroquinolone
(Ciprofloxacin) Resistance in Enterobacteriaceae from Bacteremias, England
and Wales, 19901999. EID., 8 (5): 473-478.
334. Astal Z., 2005- Increasing ciprofloxacin resistance among prevalent urinary
tract bacterial isolates in the Gaza Strip. Sing. Med. J., 46(9) : 457-460.
335. Cohen A., Calfee D., Fridkin S., et al., 2008- Recommendations for Metrics for
Multidrug-Resistant Organisms in Healthcare Settings; Infect. Con. Hosp. Epid.,
29(10): 901-913.
103
Annexes
Annex 1: Environmental and working conditions checklist
Hospital:..
Part I
Work and Treatment areas
Wards : .
Space between incubators: ...m
Area: m2
incubators:
Walls :
Ceramic
Regular painting
Notes: ..
Windows:
Blinds
curtains
Notes:
Floors:
Dining
areas:
Carpeted
Nonslip coverings
Notes:
Separate
Designated
Notes:
The staff
Main shift
Evening shift
Night shift
Total
Education and
training:
Physicians
..
..
..
..
Nurses
..
..
..
..
others
..
..
..
..
On employment
Health screening:
Annually
Immunization system:
Periodically
Upon
availability
None
documented
not documented
None
none
Environmental conditions
Ventilation:
Mechanical
Air filtration:
Natural
Present
None
Absent
Notes: ..,,,,,,
Notes: ..
Air-conditioning:
Present
Absent
Notes: ..
Monitoring,:
Documented
Not documented
None
Notes: .
Scheduled
Not Scheduled
None
Scheduled
Not Scheduled
None
manufacturers instructions
available to:
Equipment injuries:
Staff
Seniors
Documented
Head of dept
Not available
Not documented
Notes: .....
Always
On request
Availability of
antibiotics
Frequency of review
None
Local microbial
resistance data
None
Annually
Semiannually
Other
Notes: ..
..
104
Part II
Infection control team
Formation:
Physicians: .
Nurses:
Microbiologists:
Engineers:
Meetings:
Formal
Monthly
Seniors
Activities:
Further testing
of the isolates:
Informal
Weekly
Always
On request
Sometimes
105
None
On compliance
On complaint
Biweekly
None
Availability of
resources
Planned
Planned
None
Staff
Planned programs
The frequency of
sterility testing:
Others: ...
Each
Availability of infection
control manuals:
Education and training of
HCW:
Monitoring of health
status of the staff:
Epidemiologists: ...
None
None
Monthly
On suspicion
On complaint
None
Part III
Hand washing and personal hygiene
Hand washing basins
Washstands: ..
Sinks: .........
Notes: ....
Sinks Use:
Designated
General ....................
Hot and cold water
Paper towels
Antisplash devices
Disposal's sink
Hard soap
Liquid soup
Antiseptic products (formulated for use without water)
If liquid soap:
Refillable containers
Disposable cartridges
Personal protective equipment (PPE)
Gloves
Sterile gloves
Nonsterile gloves
General purpose utility gloves
Protective
Optically clear
Antifog
distortion free
Close fitting
eyewear
regular masks
Personal respiratory
protection devices
Gowns
Surgical masks
Reusable
Plastic aprons
Reusable
Footwear
Reusable
Written
Verbal
None
By hand
between workers:
Sharps trays
Puncture-proof
None
Cleaning Thermometers:
Each use
Each shift
Daily
Never
Disinfecting Thermometers:
Each use
Each shift
Daily
Never
Written
Verbal
none
Observational notes:
..
..
..
..
..
..
No special procedures
Clean
Sterile
The available
Clean
Sterile
The available
106
Part IV
Routine environmental cleaning
Written cleaning protocols:
Protocols include:
Inaccessible
areas (hard to
clean):
Routine floor
cleaning:
Written
Verbal
Few
Before each
session
None
Standard precautions
Notes:
None
After each
session
When visibly
soiled
Walls cleaning:
Daily
weekly
none
Windows cleaning:
Daily
weekly
none
Curtains cleaning:
Daily
weekly
none
Curtains changing:
Daily
weekly
none
Cleaning and
reprocessing areas
Non-defined areas
Color-coded
Gloves
Verbal
Later
Labeled
Leak-resistant bags
or containers
None
None
Neither
protective clothing
neither
Normal bags or
containers
Depending on
availability
Labeled
Not labeled
Multiple use
Daily
Weekly
Weekly
written
If present, it contains:
Personal
precautions
verbal
none
Contained
cleaning
Aerosol
prevention
Trolleys
The use of trolleys:
Cleaning of trolleys:
Weekly
107
Different uses
When visibly soiled
Source
External washstand
External medications trolley
External baby balance (Detecto)
External baby balance (shekel)
Reception washstand
Reception incubator
Internal baby balance (Detecto)
Emergency trolley
Internal reception counter
Water Bailer holder
Incubator 1 (empty)
Incubator 2
Incubator3
Incubator 4 (empty)
Incubator 5 (empty)
Incubator 6
Incubator 7
Incubator 8
Incubator 9
Incubator 10
Resuscitation unit 1
Phototherapy unit 1 (west)
Phototherapy unit 2(east)
Air condition (west) off
Air condition (northeast) on
Air condition (north east) off
Wooden table (ward center)
Internal washstand
Scrubbing 1
Scrubbing 2
Medication prep. trolley
Ambo bag (resuscitation)
Ambo bag (incubator 3)
Ambo bag (incubator 6)
Ambo bag (incubator 9)
Internal fridge
External fridge (milk)
External counter
Disposables cupboard 1
Disposables cupboard 2
Result
Enterobacter aerugenes
CoNS
Erwinia sp.
Enterobacter cloacae
Pantoea sp.
Pseudomonas sp. + CoNS
CoNS
Enterobacter sakazakii
Pantoea sp.
Pantoea sp.
CoNS
Negative
Pseudomonas sp.
Bacillus sp.
Citrobacter freundii
Pantoea sp.
Enterobacter cloacae
Pseudomonas sp.
Citrobacter freundii
Klebsiella pneumoniae
Enterobacter sakazakii
Pseudomonas sp.
Klebsiella pneumoniae
Acinitobacter sp.
Negative
Pseudomonas sp.
Pseudomonas sp. + CoNS
Serratia rupidaea
Enterobacter sakazakii
CoNS+ Bacillus sp.
Aeromonas sp.
Enterobacter cloacae + CoNS
Pseudomonas sp.
Citrobacter freundii
Aeromonas sp. + CoNS
Aeromonas sp.
Citrobacter freundii
Enterobacter cloacae
Bacillus sp.
Acinitobacter sp.
108
Result
Ground floor
Ward 2
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
109
Result
First floor
ward 1
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
61
62
63
64
65
66
67
68
69
70
Enterobacter aerugenes
Enterobacter sakazakii
Klebsiella pneumoniae
CoNS
Acinetobacter sp.
K. pneumonia
Enterobacter sakazakii
Acinetobacter sp.
Enterobacter cloacae
Enterobacter aerugenes
Negative
Enterobacter cloacae
Bacillus sp
Serratia rubidaea
CoNS + Klebsiella pneumonia
Enterobacter aerugenes
CoNS
Enterobacter sakazakii
Enterobacter cloacae
Enterobacter cloacae
Bacillus sp
Acinetobacter
Enterobacter cloacae + Bacillus sp.
Negative
Aerumonas sp.
Pseudomonas sp
Bacillus sp.
Acinetobacter sp.
Acinetobacter sp.
110
Serial:
Dear health worker: You are in direct contact with patients on a daily basis and this is why we are
interested in your opinion on health care-associated infections and hand hygiene. Your participation in
this research work will have important impact on the improvement of health care and the protection of
patients and health care workers from these infections.
Gender:
Male
12-
DOB:
/ /19
Years
Working experience:
Assistant nurse
Trainer.
Others: ..
Did you receive format training in hand hygiene in the last three years?
Yes No
Do you routinely use an alcohol-based handrub for hand hygiene?
Yes No
Profession:
Female
Physician
Nurse
handrub?
Yes
Yes
Yes
..........%
No
No
7- Do you think this research will contribute to infection control in the hospital?
8- What is the average percentage of hospitalised patients who will
Dont know
Yes
No
4- Do the patient have the right to demand you clean hands before working?
5- Do you think you are a potential source of infection?
No
Yes
No
Dont know
............%
Dont know
..........%
Can't tell
11- What do you think about the role of infection control committee in the hospital;?
Very low
Low
Moderate
High
Very high
12- What is the impact of a health care-associated infection on patient's clinical outcome?
Very low
Low
Moderate
High
Very high
13- What is the effectiveness of hand hygiene in preventing health care-associated infection?
Very low
Low
Moderate
High
Very high
High
Very high
High
Very high
Very high
Very low
Low
Moderate
Very low
Low
Moderate
16- Patients and/or their companions direct workers towards personal hygiene
Very low
Low
Moderate
High
17- The best way to make health workers comply with health conditions? (mark all that apply)
Enforcement
Promotion
Role model
111
Other:.............................
Annex 5
:
, : ,
.
. ,
. ,
.
)(........ :
:
:
..............:
:
-1
-2
-3
-4
-5
-6
-7
19 / / :
..............: ............ :
%...........
-8
%...........
-9
%...........
-14
4 3 2 1
-15
4 3 2 1
-16
4 3 2 1
-17 ) (
.................................. :
112
5
5
5
5
5
5
5
Work and
treatment areas
No. of Wards +
Resuscitation areas
Total area
No. of incubators +
resuscitation units
Space between
incubators (m)
Equipment injuries
Wall covering
Floors covering
External electrical
connections
Drinking and eating
areas
Ventilation
Filtration
Environmental
conditions
Infrastructure
maintenance &
monitoring
The staff
Antimicrobial
therapy regimen
Air condition
Monitoring of
environmental
conditions
Maintenance and
mentoring
Preventive
maintenance plan
Equip. manufactures'
instructions
Physicians/Nurses
Main shift (morning
shift)
Other shifts (evening
and night)
Education and
training
Al-Nasser NICU
Al-Shifa NICU
2+0
4+1
2
about 56 m
About 140 m2
9+2
28 + 4
0.6-1
0.6-1
Not reported
Regular painting over
cement covering
Many visible scratches
Not reported
Regular painting over
cement covering
Many visible scratches
Many
Many
No documentation
No ceramic
More scratches in
Nasser NICU
No carpets or
nonslip covering
Most of them are
external
Separated room
(designated)
None
Assumed by air
condition
2 (ground floor), 8
(upper floor)
Claimed to be done
(No documentation)
Not done
claimed to be
scheduled
Not scheduled
None
None
Upon availability
Health screening
None
Immunization
Availability of
protocols
Hepatitis B only
Reviewing the
protocols
Notes
Verbal (claimed)
None
113
No separate air
filters
Some are defected
(no regular
maintenance)
No documentation
4 physician, 6 nurses
1 physician, 4 nurses
Upon employment/
periodically
On employment (No
documentation)
Hepatitis B only
Verbal (WHO under
accreditation)
Semiannually (local
microbial resistance
data)
No documentation
No documentation
No documentation
No documentation
Annex 6 Part II
Formation
Al-Nasser NICU
1 (head of the team)
2
1
0
0
Role
Al-Shifa NICU
3 (different specialties)
3
1
0 (1 for 1meeting)
0
Pharmacist, radiologist and
an administrative
Notes
Not documented
Activities
Otters
none
Monthly
Available only for the team
Monthly
Under preparation
Claimed to be scheduled
Claimed to be scheduled
Not documented
Claimed to be scheduled
Not documented
Only on complaints
Not documented
Monthly
Monthly
-Identifying and disinfecting -Identifying and disinfecting
the infected areas
the infected areas
Testing results are used in:
-Designing and updating
-Designing and updating
infection control policies
infection control policies
1- Consolatory in both teams but more frequent in Al-Shifa team
2- Swabbing environmental spots in the section testing for contamination
No documentation
Al-Nasser NICU
Al-Shifa NICU
Hand washing is
separated from other
uses (No signs)
Available
Hard soap and liquid
soap
Refillable style
Paper towels
Not needed
Regular masks are
available but not
regularly used
Not needed
Regular masks are
available but not
regularly used
Footwear
Washstand(s)/ sink(s)
Designated use
Water mixer tap
Soap
Liquid soap containers
Towels
Gloves
Protective eyewear
Masks
114
Notes
Manual filling
Non-sterile,
sterile and
general purpose
utility
Al-Shifa NICU
notes
No written
material
Trays are
available
Instructions
Verbal
Verbal
By hand
Instructions
Verbal
Verbal
Precautions while
inserting catheters
Handwashing with
antiseptic solution is
always done.
No use of sterile gloves.
The insertion site is
cleaned with antiseptic.
The insertion site is often
dried.
The catheter is changed for
each attempt.
No special procedures
(hand washing or using
sterile gloves)
No special procedures(hand
washing or using sterile
gloves)
Direct
observations
only on suspicion
only on suspicion
Not documented
only on suspicion
Only on suspicion
Not documented
Needles disposal
Storage of sterile
equipments
Thermometers
Changing or
maintaining solution
containers, lines or
dressings
The dressing covering
the catheter
The stabilizing tape
The time and date of
insertion
Monitoring and
surveillance of
Catheter induced
infections
Testing of catheters
after use.
115
No direct
observation
No written
protocols
The information
is given by
nurses, no direct
observations
No direct
observation
No direct
observation
Annex 6 Part IV
Al-Nasser NICU
Cleaning processes
Al-Shifa NICU
notes
No written
protocols
All
equipments
are easily
removable
No rough
surfaces to
interrupt the
cleaning
process
Claims
Cleaning instructions
Verbal
Verbal
Very few
Very few
No carpets or nonslip
coverage.
Cleaned before and after
each shift and when visibly
soiled
Cleaned daily
Covered with regular
curtains
Cleaned only when visible
soil is reported, and changed
only when visibly worn-out
Defined for cleaned and
contaminated items
separately
No carpets or nonslip
coverage.
Cleaned before and after
each shift and when visibly
soiled
Cleaned daily
Covered with regular
curtains
Cleaned only when visible
soil is reported, and changed
only when visibly worn-out
Defined for cleaned and
contaminated items
separately
Verbal
Verbal
No written
protocols
Claims
Handling medical
wastes
Transport of infectious
or hazardous wastes
Cleaning of Cleaning
equipments
Changing of Cleaning
equipments
Procedural manuals
Not available
Not available
Verbal
instructions
As claimed
by senior
cleaners
The floors
The walls
The windows
The curtains
Cleaning and
reprocessing areas
Cleaning instructions
Segregation of medical
wastes from regular
wastes
Medical waste
containers
Management of
blood and body
spills
Instructions include
Use
Trolleys
Cleaning
Personal precautions
Contained cleaning
Aerosol prevention
116
Personal precautions
Contained cleaning
Aerosol prevention
No direct
observations
Bags and
containers
are not leakresistant
Claimed to be
(no signs are
noticed)
No signs
No direct
observations
No
Dk
Total
17
18
35
26
4
11
33
27
37
37
37
28
34
36
Question content
37
37
37
Part II
Question content
8- Average percentage of HAI
9- Colleagues commitment to PHP
10- Respondent's commitment to PHP
HAI= health care-Associated infection
Dk= dont know or dont remember
Dk
<30%
30-50%
>50%
29
2
4
2
19
0
6
11
13
0
3
21
PHP= Personal Hygiene Practices
Total
37
36
37
Part III
Question content
total
2
18
12
5
0
1
5
12
14
5
0
1
4
14
18
2
11
10
11
2
3
10
13
10
1
3
9
14
8
3
4
18
10
4
0
1= very low, 2= low, 3= moderate,
4= high, 5= very high
37
37
37
36
37
35
36
Part VI
Question content
17- The best way to make health workers comply with health conditions
9
29
11
41-4
A= Enforcement
B= Promotion
C= Role model
D= Further suggestions
1
Punishment and criticism, 2conscious, 3continuous education of the workers about the importance of the
compliance to the patient and to himself and 4periodical examining of workers and the punishment for
those who dont comply
117
Ward
Al-Nasser
Main
Resuscitation
Reception
Ground
floor
West
Resuscitation
First floor
Al-Shifa
1.
2.
3.
East
East
West
Bacteria 1,2
Count
Mean
67
63
91
124
110
63
115
108
100
90
85
81
85
90
95
77
89
99
82
56
83
79
81
79
84
71
Fungi1.3
Count
mean
21
17
18
10
25
30
25
25
25
16
25
33
29
26
23
26
21
22
21
22
18
19
17
19
21
19
CFU/50Litres
2 days incubation on nutrient agar
5 days incubation on Dichloran Rose Bengal Chloramphenicol Agar (DRBC Agar)
118
Annex 9: Antibiotic sensitivity for selected Gram negative bacteria isolated from
blood culture, environment, hand and nasal swabs.
Na
Cp
119
Te
Enterobacter cloacae
I
R
S
S
S
R
I
S
R
R
R
S
S
S
R
I
S
R
I
R
S
S
S
R
S
S
R
R
R
R
S
S
R
R
R
S
R
I
S
S
S
R
R
R
R
R
R
S
S
S
R
R
R
S
R
R
S
S
S
R
R
R
R
R
S
S
S
R
R
R
S
R
R
S
S
S
R
R
R
S
I
R
R
S
S
S
R
R
R
S
R
S
S
S
R
R
R
S
R
R
S
S
S
R
R
R
S
S
R
S
S
S
S
R
I
S
S
R
S
S
S
S
R
S
S
I
S
S
S
S
S
R
S
S
S
R
S
S
S
S
R
S
S
I
I
S
S
S
R
R
R
S
S
R
R
S
S
S
R
R
R
S
I
R
S
S
S
R
R
R
S
R
S
S
S
S
R
R
R
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
R
S
S
S
S
S
S
S
S
R
S
S
S
S
S
S
S
S
R
R
S
S
R
R
S
S
S
R
R
R
R
S
S
S
S
S
R
S
S
S
S
S
S
S
R
S
S
S
I
S
S
S
S
S
R
S
S
S
S
S
S
S
R
S
S
S
I
R
R
S
S
R
R
R
S
R
S
S
S
S
R
S
S
S
S
S
S
S
S
S
R
S
S
I
S
S
S
S
S
S
S
S
S
S
S
S
S
R
S
S
S
S
R
R
S
S
R
R
R
R
R
S
S
S
S
R
S
S
S
S
Am=ampicillin, PIP=piperacillin, GM=gentamicin,
Ak=amikacin, MEM=meropenem, I=imipinem, Cn=
Cephalexin, Cfm= cefixime, CRO=ceftriaxone,
C=chloramphenicol, TR=trimethoprim, Te=tetracycline,
Na=nalidixic acid, Cp= ciprofloxacin
TR
Cro
Cfm
Cn
MEM
Eschericiha
coli
ShE33
ShE44
ShE47
ShE56
ShH17
ShH18
NsE20
NsE23
NsH02
NsN11
ShB21
ShB22
ShE13
ShE31
ShN14
ShB07
ShB20
ShE05
ShE23
ShE50
ShE53
ShE60
ShE61
ShE64
ShH04
NsB24
NsE04
NsE17
NsE32
NsE38
Sh=Al-Shifa NICU,
Ns=Al-Nasser NICU,
B=blood, H=hand,
N=nasal,
E=environmental
Ak
R
R
R
R
R
R
R
R
R
R
R
R
R
R
I
R
S
R
R
R
S
R
R
R
R
R
R
R
R
R
R
R
S
R
R
S
GM
ShB01
ShB02
ShB09
ShE04
ShE11
ShE24
PIP
Klebsiella pneumoniae
Source
Am
Bacteria
Antibiotic sensitivity
R
R
R
R
R
R
R
R
R
R
R
R
S
S
S
S
R
R
S
R
R
S
R
S
R
I
S
R
S
R
S
S
S
S
R
S
I
S
S
S
R
S
I
R
S
S
S
I
S
S
S
I
I
R
I
S
S
S
S
S
S
I
I
R
S
S
S
I
S
S
I
S
S
S
R
R
S
S
R
S
S
I
S
S
S
R
R
S
R
R
I
S
S
S
R
R
R
S
S
S
S
S
S
S
S
S
S
S
I
I
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
R
S
S
S
S
S
S
S
S
S
R
S
S
S
S
S Sensitive
I Intermediate
R Resistant
Am
PIP
Cn
Cfm
Cro
GM
Ak
MEM
TR
Va
Cp
Tet
01
SB03
02
SB08
03
SB10
04
SB23
05
SB24
06
SN01
07
SN02
08
SN03
09
SN08
10
11
SN10
NB02
12
NB04
13
NB05
14
NB08
15
NB09
16
NB10
17
NB12
18
NB13
19
NB14
20
NB16
21
NB17
22
NB18
23
NB21
24
NB23
25
NB25
26
NH04
27
NH15
28
NH07
29
NN04
30
NN05
31
NN06
32
NN09
R
Sh=Al-Shifa NICU,
Ns=Al-Nasser NICU,
B=blood,
H=hand,
N=nasal,
E=environmental,
A=air
S S R S S S S S S S S S S S
P=penicillin, Am=ampicillin,
S Sensitive
I Intermediate
PIP=piperacillin, Cn= Cephalexin , Cfm=
R Resistant
cefixime, CRO=ceftriaxone,
GM=gentamicin, Ak=amikacin,
I=imipinem, MEM=meropenem,
TR=trimethoprim, Va=vancomycin, Cp=
ciprofloxacin C=chloramphenicol,
Te=tetracycline, E=erythromicin
120
Am
PIP
Cn
Cfm
Cro
GM
Ak
Tm
Va
Cp
Tet
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
Code
SA02
SA09
SA13
SA19
SA21
SA25
SB04
SB04
SB11
SB12
SB16
SB18
SB25
SE30
SE45
SE56
SE58
SH10
SH12
SH15
SN04
SN06
SN07
SN09
SN12
SN13
SN17
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
S
S
R
R
R
R
R
R
R
S
R
S
R
S
R
R
R
R
S
R
R
S
R
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
I
I
R
R
R
S
S
S
R
S
I
R
R
R
S
S
S
S
S
S
S
R
R
R
R
R
R
R
R
R
R
R
R
S
R
R
R
R
R
R
R
R
R
R
R
R
R
R
S
S
S
I
S
S
I
I
I
R
I
I
S
S
S
S
S
R
R
S
S
S
I
R
S
S
S
S
R
S
R
S
S
S
S
S
R
R
S
S
S
S
S
S
R
S
S
S
S
S
I
S
S
S
S
S
S
S
S
S
R
R
I
R
R
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
I
R
I
I
S
S
R
R
R
R
R
R
I
I
S
S
R
R
R
R
S
R
R
R
R
S
R
S
R
S
S
S
I
R
R
R
R
S
R
R
S
R
R
R
S
R
R
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
I
R
R
S
S
S
S
S
S
S
S
S
S
S
S
S
R
S
S
S
S
S
S
S
S
S
S
S
S
S
R
S
S
S
S
S
R
S
S
S
S
S
S
S
S
S
I
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
I
S
R
S
S
S
S
R
S
S
S
R
R
R
R
I
R
R
R
R
R
R
R
I
S
S
S
I
R
R
I
I
I
S
R
R
I
R
B=blood,
H=hand,
N=nasal,
E=environmental,
A=air
121
S Sensitive
I Intermediate
R Resistant
Am
PIP
Cn
Cfm
Cro
GM
Ak
Tm
Va
Cp
Tet
01
02
03
04
05
06
07
08
09
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
Code
NA02
NA08
NA09
NA13
NB03
NB06
NB07
NB11
NB19
NB20
NB22
NE02
NE06
NE07
NE11
NE27
NE30
NE32
NE35
NH03
NH05
NH09
NH17
NN02
NN16
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
S
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
S
S
S
R
R
R
R
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
R
R
R
R
R
R
R
S
S
S
S
S
S
S
S
S
S
R
S
S
S
S
S
S
S
R
R
R
R
R
R
R
S
S
S
S
S
S
S
S
S
S
R
S
S
S
I
S
S
S
I
I
I
I
R
R
R
S
S
S
S
S
S
S
S
I
S
R
S
S
S
R
S
R
S
S
S
S
S
I
I
R
S
S
S
S
S
S
S
S
S
S
S
I
S
S
R
S
S
S
S
S
S
S
R
R
R
S
S
S
S
S
S
S
S
S
S
S
I
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
R
R
R
I
R
R
R
R
R
S
S
R
R
R
R
R
R
R
R
R
S
R
R
R
R
R
I
R
S
R
R
R
R
R
R
R
R
R
R
R
R
R
R
R
S
R
R
S
R
R
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
R
R
R
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
R
S
S
S
S
S
S
S
R
S
S
S
S
S
S
S
S
R
S
S
S
S
S
S
S
R
S
S
S
I
S
S
S
S
S
S
I
S
R
S
S
S
R
I
R
R
S
I
I
I
R
R
R
R
I
R
I
R
R
R
R
S
I
S
S
S
S
B=blood,
H=hand,
N=nasal,
E=environmental,
A=air
122
S Sensitive
I Intermediate
R Resistant
123