Sakazakii Infection Research Articles

Restructuring the FDA's Food Program: Promises and Pitfalls.

Following an outbreak of Cronobacter sakazakii infection in infant formula, the US Food and Drug Administration commissioned a series of reports and then undertook a major reorganization of its food program. This article describes the changes that went into effect on 1 October 2024, why those changes are likely to improve the new Human Foods Program, and additional work that must be undertaken to enhance the agency's impact upon public health.

Subtractive genomics study for the identification of therapeutic targets against Cronobacter sakazakii: A threat to infants

Cronobacter sakazakii is an opportunistic pathogen that has been associated with severe infection in neonates such as necrotizing enterocolitis (NEC), neonatal meningitis, and bacteremia. This pathogen can survive in a relatively dry environment, especially in powdered infant formula (PIF). Unfortunately, conventional drugs that were once effective against C. sakazakii are gradually losing their efficacy due to rising antibiotic resistance. In this study, a subtractive genomic approach was followed in order to identify potential therapeutic targets in the pathogen. The whole proteome of the pathogen was filtered through a step-by-step process, which involved removing paralogous proteins, human homologs, sequences that are less essential for survival, proteins with shared metabolic pathways, and proteins that are located in cells other than the cytoplasmic membrane. As a result, nine novel drug targets were identified. Further, the analysis also unveiled that the FDA-approved drug Terbinafine can be repurposed against the Glutathione/l-cysteine transport system ATP-binding/permease protein CydC of C. sakazakii. Moreover, molecular docking and dynamics studies of Terbinafine and CydC suggested that this drug can be used to treat C. sakazakii infection in neonates. However, for clinical purposes further in vitro and in vivo studies are necessary.

Cronobacter sakazakii infection implicates multifaceted neuro-immune regulatory pathways of Caenorhabditis elegans.

The neural pathways of Caenorhabditis elegans play a crucial role in regulating host immunity and inflammation during pathogenic infections. To understand the major neuro-immune signaling pathways, this study aimed to identify the key regulatory proteins in the host C. elegans during C. sakazakii infection. We used high-throughput label-free quantitative proteomics and identified 69 differentially expressed proteins. KEGG analysis revealed that C. sakazakii elicited host immune signaling cascades primarily including mTOR signaling, axon regeneration, metabolic pathways (let-363 and acox-1.4), calcium signaling (mlck-1), and longevity regulating pathways (ddl-2), respectively. The abrogation in functional loss of mTOR-associated players deciphered that C. sakazakii infection negatively regulated the lifespan of mutant worms (akt-1, let-363 and dlk-1), including physiological aberrations, such as reduced pharyngeal pumping and egg production. Additionally, the candidate pathway proteins were validated by transcriptional profiling of their corresponding genes. Furthermore, immunoblotting showed the downregulation of mTORC2/SGK-1 during the later hours of pathogen exposure. Overall, our findings profoundly provide an understanding of the specificity of proteome imbalance in affecting neuro-immune regulations during C. sakazakii infection.

Urinary Tract Infection by Enterobacter sakazakii: A Case Report

Introduction: Enterobacter sakazakii is considered a rare yet extremely important cause of enterocolitis and may lead to a necrotizing condition. Central nervous system and blood infections with this type of organism will be fatal, with a mortality rate of as much as 40 - 80%. Case Presentation: Our case report is a 31-month-old boy with a history of posterior urethral valves surgery presented to the emergency department with a history of dysuria, dribbling, and a 24-hour history of fever, chill, and anorexia. The case had a urinary tract infection diagnosis with E. sakazakii. Conclusions: E. sakazakii can cause bacteremia, meningitis, and necrotizing enterocolitis, but E. sakazakii causes rare literature about urinary tract infection (UTI). We have reported a rare Enterobacter sakazakii infection in the present study.

Antibiotic treatment during post-natal reverses behavioural and molecular alterations in experimental meningitis survivor rat model

The present study was aimed to examine the behavioural and molecular alterations in experimental meningitis survivor rat model. On postnatal day (PND)-2, animals were assigned to different groups: (i) Control (Ctrl), (ii) Positive Control [PCtrl: gavaged with Luria-Bertani (LB) broth on PND-2 and received antibiotics treatment (AbT) from PND-5 to 11], (iii) Cronobacter sakazakii (CS: received single dose of live bacterial culture on PND-2) infected. Later, a subset of CS group received antibiotics treatment (AbT) from PND-5 to 11 and assigned as group (iv) (CS + AbT/ survivor). On PND-35, animals were subjected to behavioural tasks [viz., elevated plus maze (EPM) test and step-through inhibitory retention], and sacrificed for molecular analyses. We found that CS infection induces anxiety-like behaviour, impaired short/long-term memory and differentially altered the expression of brain-derived neurotrophic factor (BDNF) splice variants (III, IV and VI), decreased expression of BDNF, Src family tyrosine kinase (FYN), focal adhesion kinase (FAK) and nerve growth factor (NGF). The observed behavioural phenotype and expression pattern of candidate genes fit in the correlation. In addition, NGF expression was reduced in dentate gyrus (DG) and CA1 regions of hippocampus. Notably, antibiotic treatment reduced the anxiety-like behaviour, improved step-through inhibitory retention and suppressed infection induced reduction in BDNF, FYN, FAK and NGF expressions in survivors, however, not comparable to the control group. Overall, our experimental meningitis survivor model demonstrate that antibiotic treatment minimize the C. sakazakii infection induced effect on behaviour and signaling molecules involving in neuronal development, survival, and synaptic plasticity, but the consequences are long-term.

Foodborne pathogens in Africa: Understanding Cronobacter sakazakii

AbstractCronobacter sakazakii is an emerging and opportunistic foodborne pathogen that causes severe infantile diseases, including meningitis, necrotizing enterocolitis, and septicemia. It has been reported in numerous countries around the world, including those in Africa. Although it has been isolated from food, environmental and clinical samples across Africa, the most implicated source of the C. sakazakii infection outbreaks across the globe has been the consumption of contaminated powdered infant formula. Cronobacter has many unique characteristics that contribute to its survival in harsh environments and transmission along the food chain from production to consumption. A potential foodborne disease outbreak caused by C. sakazakii can increase the overall foodborne disease burden and hinder any progress in managing the overly strained public health situation in Africa. This article presents an insight into the occurrence and prevalence of C. sakazakii infection in Africa's food environment, pointing out the transmission route along the food chain and its accompanying food safety concerns. This paper advocates for strict compliance with food safety and control measures to prevent its spread in African countries.

Reduced Reelin Expression Induces Memory Deficits through Dab-1/ NMDAR Signaling Pathway: Cronobacter sakazakii Infection in a Rat Model of Experimental Meningitis

The purpose of this study was to examine whether the Cronobacter sakazakii infection-induced inflammation alters the Reelin signaling pathway that is involved in learning and memory. To test this, postnatal day (PND)-15 rat pups were either treated with Luria Bertani broth/Escherichia coli OP50/C. sakazakii through oral gavage or maintained as control and allowed to stay with their mothers until PND-24. Experimental groups’ rats were subjected to long-term novel object recognition test during their adolescent age PND-30–32. Observed behavioral data showed that C. sakazakii infection causes a deficit in recognition of novel objects from known objects. Further, our analysis showed that C. sakazakii infection-mediated inflammation decreases the Reelin expression by proteolytic cleavage and alters its receptor apolipoprotein E-receptor (ApoER)-2 splice variants ApoER2 (ex19) and ApoER2 (Δ). Subsequently, downregulated Reelin alters the phosphorylation of disabled adapter protein (Dab)-1 and leads to differential expression of N-methyl-D-aspartate (NMDA) receptor subunits 2A and 2B. Further, the NMDA receptor influences the expression of postsynaptic density (PSD)-95 protein and brain-derived neurotrophic factor (BDNF). Observed results suggest a deficit in recognition of novel objects possibly due to the alternation in Reelin signaling pathway.

Physiological and Metabolite Alterations Associated with Neuronal Signals of Caenorhabditis elegans during Cronobacter sakazakii Infections.

Metabolomic reprogramming plays a crucial role in the activation of several regulatory mechanisms including neuronal responses of the host. In the present study, alterations at physiological and biochemical levels were initially assessed to monitor the impact of the candidate pathogen Cronobacter sakazakii on the nematode host Caenorhabditis elegans. The abnormal behavioral responses were observed in infected worms in terms of hyperosmolarity and high viscous chemicals. The microscopic observations indicated reduction in egg laying and internal hatching of larvae in the host. An increased level of total reactive oxygen species and reduction in antioxidant agents such as glutathione and catalase were observed. These observations suggested the severe effect of C. sakazakii infection on C. elegans. To understand the small molecules which likely mediated neurotransmission, the whole metabolome of C. elegans during the infection of C. sakazakii was analyzed using liquid chromatography-mass spectrometry. A decrease in the quantity of methyl dopamine and palmitoyl dopamine and an increase in hydroxyl dopamine suggested that reduction in dopamine reuptake and dopamine neuronal stress. The disordered dopaminergic transmission during infection was confirmed using transgenic C. elegans by microscopic observation of Dat-1 protein expression. In addition, reduction in arachidonic acid and short-chain fatty acids revealed their effect on lipid droplet formation as well as neuronal damage. An increase in the quantity of stearoyl CoA underpinned the higher accumulation of lipid droplets in the host. On the other hand, an increased level of metabolites such as palmitoyl serotonin, citalopram N-oxide, and N-acyl palmitoyl serotonin revealed serotonin-mediated potential response for neuroprotection, cytotoxicity, and cellular damage. Based on the metabolomic data, the genes correspond to small molecules involved in biosynthesis and transportation of candidate neurotransmitters were validated through relative gene expression.

Comparison between Preterm versus Full Term Septic Neonates Whose Feeding Is Powdered Milk Formula Regarding Cronabacter Sakazakii

Background: Foodborne pathogen Cronobacter sakazakii (CS) has been detected around the world. When it comes to foodborne bacteria, C. difficile (CS) is one of the most prevalent diseases, particularly among infants with low birth weight and preterm neonates. Objective: To compare between the incidence of Cronobacter Sakazakii infection among preterm versus full term septic neonates whose feeding is powdered milk formula. Patients and Methods: Our study was a comparative cross-sectional study and included 50 neonates: 25 full term and 25 premature. It was conducted at Pediatrics Department, Zagazig University Hospital and the patients’ status fulfilled the inclusion and exclusion criteria. Medical history, clinical examination, and laboratory tests were performed on all patients. Collection of specimens and culture and sensitivity tests for the isolates were also done. Results: There was significant increase of prevalence of Cronobacter sakazakii in preterm more than full term. The sepsis score and its associated characteristics varied significantly between the two groups. With time, increasing temperature led to reduce number of C. sakazakii in reconstituted infant powdered milk Conclusion: Powdered infant formula (PIF) can be contaminated with C. sakazakii, which can cause sickness in infants who are fed PIF rather than breast milk, and in preterm infants rather than full-term ones.

Infection of Cronobacter sakazakii ST1 Producing SHV-12 in a Premature Infant Born from Triplet Pregnancy

Cronobacter sakazakii can cause severe life-threatening invasive infections in neonates, with a high mortality rate mostly associated with powdered infant formula consumption. The study describes a fatal C. sakazakii infection in premature infant fed only with expressed human milk. Despite the identification of etiological factor from patient’s blood, the epidemiological investigation, including mother’s skin, hospital surfaces, milk expressing devices, and milk samples, did not show bacterial contamination. The infection was caused by C. sakazakii ST1, being one of the leading genotypes reported in invasive infections. The phylogenetic analysis of the international collection of the ST1 organisms allowed us to identify the isolate as a member of the main cluster. The pathogenic potential of the isolate was augmented by the presence of IncFIB-like molecule representing virulence plasmids of pESA-3 family. Isolate presented ESBL phenotype associated with blaSHV-12 gene harboured by IncX3 plasmid. The described case gave valuable information to genetics of Cronobacter, and also urges the need of wider whole-genome sequencing implementation as a part of diagnostic procedure.

Cronobacter sakazakii ATCC 29544 Translocated Human Brain Microvascular Endothelial Cells via Endocytosis, Apoptosis Induction, and Disruption of Tight Junction.

Cronobacter sakazakii (C. sakazakii) is an emerging opportunistic foodborne pathogen that can cause neonatal necrotizing enterocolitis, meningitis, sepsis in neonates and infants with a relatively high mortality rate. Bacterial transcytosis across the human brain microvascular endothelial cells (HBMEC) is vital for C. sakazakii to induce neonatal meningitis. However, few studies focus on the mechanisms by which C. sakazakii translocates HBMEC. In this study, the translocation processes of C. sakazakii on HBMEC were explored. C. sakazakii strains could effectively adhere to, invade and intracellularly survive in HBMEC. The strain ATCC 29544 exhibited the highest translocation efficiency across HBMEC monolayer among four tested strains. Bacteria-contained intracellular endosomes were detected in C. sakazakii-infected HBMEC by a transmission electron microscope. Endocytosis-related proteins CD44, Rab5, Rab7, and LAMP2 were increased after infection, while the level of Cathepsin L did not change. C. sakazakii induced TLR4/NF-κB inflammatory signal pathway activation in HBMEC, with increased NO production and elevated mRNA levels of IL-8, IL-6, TNF-α, IL-1β, iNOS, and COX-2. C. sakazakii infection also caused LDH release, caspase-3 activation, and HBMEC apoptosis. Meanwhile, increased Dextran-FITC permeability and decreased trans epithelial electric resistance indicated that C. sakazakii disrupted tight junction of HBMEC monolayers, which was confirmed by the decreased levels of tight junction-related proteins ZO-1 and Occludin. These findings suggest that C. sakazakii induced intracellular bacterial endocytosis, stimulated inflammation and apoptosis, disrupted monolayer tight junction in HBMEC, which all together contribute to bacterial translocation.

Pyosalpinx due to Cronobacter sakazakii in an elderly woman

BackgroundCronobacter sakazakii (C. sakazakii) is a bacterium known to cause severe neonatal infections in premature infants with the consumption of contaminated powdered milk formula. Adult infections are rare, and there have been no reports of pyosalpinx due to C. sakazakii to date.Case presentationWe report a case of left pyosalpinx due to C. sakazakii in a sexually inactive postmenopausal woman. A 70-year-old woman presented to our hospital with left lower abdominal pain and fever. Abdominal computed tomography disclosed a cystic mass continuous with the left edge of the uterus. Urgent laparotomy revealed a ruptured left pyosalpinx with pus-like content. Left salpingo-oophorectomy, resection of the right tube, and washing of the abdominal cavity with saline were performed. Pathological examination of the left adnexa showed tubal tissue with acute inflammation and inflammatory exudate, which were compatible with pyosalpinx, and pus culture yielded C. sakazakii.ConclusionsThis is the first case report of pyosalpinx due to C. sakazakii. Cronobacter sakazakii infections in adult women might occur in the elderly, whose immunity has weakened. Further accumulation of cases of C. sakazakii infection is needed to clarify the etiology and behavior of C. sakazakii in adults.

Cronobacter Sakazakii: A Foodborne Pathogenic Bacterium in Immunocompromised and Hospitalized Patients

Aims: Cronobacter sakazakii (CS) is a member of the Enterobacteriaceae family. It is a genomically heterogeneous, motile, Gram-negative bacillus. It is also an emergent foodborne pathogen associated with the ingestion of infant formula milk that can cause neonatal sepsis, necrotizing enterocolitis, and meningitis. This review is focused on the newest information about the bacterial characteristics of C. sakazakii and human infections causing by this pathogenic bacterium. Methods & Materials: We searched medical databases such as ISI Web of Science, PubMed, Scopus, and other websites. Findings: Cronobacter sakazakii acts as a microbiological hazard in the infant food chain, with historic high mortality in neonates. The International Commission for Microbiological Specifications for Foods has categorized C. sakazakii as a severe hazard bacterium for some individuals, with long duration, substantial chronic sequelae, or life-threatening complications. Although the incidence of C. sakazakii infection is low, the prognosis of the disease is poor, and infection is associated with significant morbidity and mortality. Powdered Infant Formula (PIF) milk products contaminated with C. sakazakii have been epidemiologically linked to several clinical cases. Premature infants, low-birth-weight ones, and patients hospitalized in the Neonatal Intensive Care Units (NICUs) are more at infection risk than older infants. Conclusion: We recommend focusing on simple preventative strategies such as the promotion of breast milk feeding, the inclusion of warnings on the powder infant formula packages that may be contaminated with C. sakazakii, and abstinence from the practice of re-warming of reconstituted formula. Reconstituted dairy products should be avoided in adult immunosuppressed populations. Appropriate barrier precautions should be observed in NICU and intensive care unit settings, where the spread of infection may be more prevalent.

Cronobacter sakazakii Infection in Early Postnatal Rats Impaired Contextual-Associated Learning: a Putative Role of C5a-Mediated NF-κβ and ASK1 Pathways.

This study was designed to test whether the Cronobacter sakazakii infection-impaired contextual learning and memory are mediated by the activation of the complement system; subsequent activation of inflammatory signals leads to alternations in serotonin transporter (SERT). To test this, rat pups (postnatal day, PND 15) were treated with either C. sakazakii (107CFU) or Escherichia coli OP50 (107CFU) or Luria bertani broth (100μL) through oral gavage and allowed to stay with their mothers until PND 24. Experimental groups' rats were allowed to explore (PNDs 31-35) and then trained in contextual learning task (PNDs 36-43). Five days after training, individuals were tested for memory retention (PNDs 49-56). Observed behavioural data showed that C. sakazakii infection impaired contextual-associative learning and memory. Furthermore, our analysis showed that C. sakazakii infection activates complement system complement anaphylatoxin (C5a) (a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS1)) and mitogen-activated protein kinase kinase1 (MEKK1). Subsequently, MEKK1 induces pro-inflammatory signals possibly through apoptosis signal-regulating kinase-1 (ASK-1), c-Jun N-terminal kinase (JNK1/3) and protein kinase B gamma (AKT-3). In parallel, activated nuclear factor kappa-light-chain-enhancer B cells (NF-κB) induces interleukin-6 (IL-6) and IFNα-1, which may alter the level of serotonin transporter (SERT). Observed results suggest that impaired contextual learning and memory could be correlated with C5a-mediated NF-κβ and ASK1 pathways.

Inhibition of Cronobacter sakazakii in reconstituted infant formula using triglycerol monolaurate and its effect on the sensory properties of infant formula

Cronobacter sakazakii (C. sakazakii) is an opportunistic foodborne pathogen in infant formula. This study was designed to explore the inhibitory effect of TGML on C. sakazakii in reconstituted infant formula (RIF). Firstly, the growth curve of C. sakazakii in RIF treated by TGML and the effect of different temperatures (4, 10, 21, 30 and 37 °C), pH values (5, 6, 7, 8 and 9) and ionic strengths (25, 50, 100, 200, 400 and 800 mM) on its activity were assessed. The results showed that the inhibitory effect of TGML on C. sakazakii was dose-dependent, and 1, 2 and 5 μg/mL TGML delayed the visible growth of pathogen by 4, 12 and 24 h, respectively. Storage temperature above or below room temperature enhanced the bioactivity of TGML. And a decrease in pH also increased the antibacterial effect of TGML. However, the effect of ionic strength on its activity was not obvious. Subsequently, the antibacterial effect of TGML in physiological gastric acid and simulated gastric juice in vitro was further explored. We found that only 5 μg/mL TGML could inhibit the growth of pathogen below the infectious dose (10,000 CFU in total) in simulated gastric juice during the whole gastric emptying period (3.5–21 h), weaker than its antibacterial effect in physiological gastric acid and room temperature culture. Finally, the effect of TGML and the above environmental factors on the color and aroma of infant milk was evaluated by a 12-person panel. The results revealed that TGML did not affect the sensory flavor of milk, and the color and odor scores of infant milk under different environmental conditions did not show any significant differences. Therefore, it is concluded that TGML has a good inhibitory effect on C. sakazakii in RIF and a high sensory acceptability for consumers. Adjusting the temperature or lowering the pH enhances its bacteriostatic activity. However, the presence of infant gastric juice can impair the bioactivity of TGML. Overall, this study will provide some new ideas for controlling and eliminating the potential risk of C. sakazakii infection during infant feeding.

Citral Attenuated Intestinal Inflammation Induced by Cronobacter sakazakii in Newborn Mice.

Necrotizing enterocolitis (NEC) is a serious inflammatory intestinal disorder with a high mortality rate, which occurs most commonly in newborn infants. Cronobacter sakazakii, a common contaminant in infant formula, is associated with NEC. However, its role in NEC pathogenesis is unknown, and there are still no effective treatments for NEC. Currently, natural bioactive products have been investigated for their beneficial effects in preventing microbial infection. In this study, a neonatal mouse intestinal inflammation model was used to examine the protective effects of citral (a natural bioactive product) on C. sakazakii-induced intestinal inflammation and damages. It was shown that citral reduced the number of C. sakazakii cells in ileal tissues, and mice treated with citral had a significantly higher body weight than C. sakazakii-infected mice. Citral treatment also ameliorated serious ileal tissue damages, including epithelial sloughing, villous rupture, and enterocyte apoptosis. C. sakazakii infection upregulated the messenger RNA transcription levels of several inflammation-associated genes, increased production of IL-6 and TNF-α, and activated the NF-κB and MAPK signaling pathways in ileal tissues. Citral treatment mitigated these inflammatory responses. The apoptotic index and activities of caspase 3, 8, and 9 increased in murine ileum after C. sakazakii infection, but citral inhibited both enterocyte apoptosis and activations of these caspase. These findings suggest that citral has protective effects on C. sakazakii-induced intestinal inflammation in newborn mice, and it may play a future role in the management of C. sakazakii-associated infections and diseases.

Evaluation of Cronobacter sakazakii inactivation and physicochemical property changes of non-fat dry milk powder by cold atmospheric plasma

Cronobacter sakazakii can cause life-threatening infections in neonates. Exposure to contaminated powdered food, especially milk powder, is a major route for C. sakazakii infection. Cold atmospheric plasma (CAP) is well known as a non-thermal method for inactivating microbial pathogens. This study evaluates the effectiveness of CAP on C. sakazakii in non-fat dry milk (NFDM) powder using a fluidized reaction system. The CAP treatments for 20–120 s led to 1.17–3.27 log10 reductions of C. sakazakii. C. sakazakii inactivation increased with increasing flow rate from 8 to 20 L/min. In terms of quality attributes of NFDM after the CAP treatments, no noticeable color changes (ΔE < 1.5) were observed. Moreover, no significant changes in crystallinity, amino acid composition, or phenolic content occurred following a 120s-CAP treatment. These results indicate that this fluidized reaction system combined with CAP can provide an effective antimicrobial activity with minimal effects on some physicochemical properties of NFDM powder.

Effects of intense pulsed light on Cronobacter sakazakii inoculated in non-fat dry milk

Cronobacter sakazakii is known to have caused life-threatening infections in neonates with a fatality rate of 40–80%. Contaminated powdered food, especially powdered infant formula (PIF), has been epidemiologically linked with these foodborne outbreak infections. Clinical symptoms of C. sakazakii infection include necrotizing enterocolitis, bacteremia, and meningitis. Traditional thermal processing of PIF has been used to kill foodborne pathogens, but it has an undesirable flavor and quality attributes that are unacceptable for industrial usage. Thus, there is a need for new bactericidal technologies for dry powdered foods. In this study, an intense pulsed light (IPL) treatment system was developed, and processing parameters such as relative humidity, environmental temperature, initial water activity, initial temperature, and residence time were evaluated for a bactericidal effect on C. sakazakii in non-fat dry milk (NFDM). The results indicated that a synergistic effect of IPL and an appropriate temperature of ∼57.5 ± 0.7 °C exhibited maximum inactivation of 3.18 log10 CFU/g for C. sakazakii in NFDM with little agglomeration at the initial temperature of 25 °C, at the water activity level of 0.25, and a residence time of 28 s. In addition, significantly higher inactivation was observed when IPL was combined with a vibratory feeder (p < 0.05). No significant change in the amino acid composition, particle physical appearance, and typical volatile compounds were observed after IPL treatment. Overall, the study demonstrates that IPL treatment is promising for inactivation of C. sakazakii in NFDM with minimal quality degradation.

Notes From the Field: Cronobacter sakazakii Infection Associated With Feeding Extrinsically Contaminated Expressed Human Milk to a Premature Infant—Pennsylvania, 2016

Notes From the Field: Cronobacter sakazakii Infection Associated With Feeding Extrinsically Contaminated Expressed Human Milk to a Premature Infant—Pennsylvania, 2016

First Detection of Augmentin and Colistin Resistant &amp;lt;i&amp;gt;Cronobacter Sakazakii&amp;lt;/i&amp;gt; from a Pharmaceutical Wastewater in South-Western Nigeria

Cronobacter sakazakii formerly known as Enterobacter sakazakii, is a bacterium with a rare cause but often fatal infection of the bloodstream and central nervous system. Infants with weakened immune systems, particularly premature infants, are most likely to contact a Cronobacter infection, although the bacteria have caused illnesses in all age groups. Most cases of C. sakazakii infection come from powdered infant formula (PIF) contaminated with the bacterium. Although relatively little information is known about the existence of Cronobacter in the environment, more reservoirs are being identified, such as water, soil and plant material. Wastewaters from 6 pharmaceutical industries located in a south-western state in Nigeria were sampled and analyzed. Bacteria were isolated using standard methods and species identification was determined by Gram staining, lactose fermentation, oxidase, catalase and Vitek 2. Antibacterial susceptibility to 25 antimicrobial agents was tested by the disc diffusion method and Vitek 2. Fifty nine Gram-negative bacteria were isolated and identified; one was identified as C. sakazakii. The bacterium was susceptible to all antibiotic mentioned but resistant to augmentin (amoxicillin/clavulanate) and colistin which are high potent drugs for the treatment of very stubborn infections. The public health implication of this fact is that this bacterium could be harbouring resistant genes that can be transferred through water ways such as the pharmaceutical wastewaters to bacteria of the same or different species of clinical importance. Therefore, continuous surveillance of the environmental reservoirs of antibiotic resistant bacteria is necessary to prevent their further spread.