Nontyphoidal Salmonella Enterica Meningitis in an Infant: A Case Report
Yaser Ali 1, Mohamed Elkafafi 2*, Hussein Hamed 3, Ahmed Attia 4, Ahmed Ghorab 5,
Nitin Pathare 6, Rajesh Phatak 7
1,2,3,4,6,7. Burjeel Hospital, Abu Dhabi, United Arab Emirates
5. East Lancashire NHS Trust, United Kingdom.
*Correspondence to: Mohamed Elkafafi. Burjeel Hospital, Abu Dhabi, United Arab Emirates.
Copyright
© 2026: Mohamed Elkafafi. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Received: 05 October 2026
Published: 01 November 2026
DOI: https://doi.org/10.5281/zenodo.23337874
Nontyphoidal Salmonella meningitis is a severe and rare invasive infection in infants, which is linked to a high morbidity and neurological sequelae. A 4-month-old patient with an underlying immune disorder was reported with 5 days of fever, diarrhea, irritability, poor feeding, and lethargy. The patient was initially diagnosed with gastroenteritis, and no response was observed after treatment. The patient was referred to the pediatric intensive care unit, with a temperature of 38 °C, blood pressure of 85/ 85/45 mmHg, and a Glasgow Coma Scale of 13/15. The levels of inflammatory markers were highly expressed (CRP 305 mg/dL, procalcitonin 35.5 ug/L). The first cerebrospinal fluid contained 340 cells/cmm, protein 247 mg/DL, and glucose 0.38 mmol/L with gram-negative rods. Blood and CSF cultures were positive for nontyphoidal Salmonella that is sensitive to ceftriaxone and meropenem. MRI revealed several rim-enhancing lesions, leptomeningeal enhancement, vasculitis, and acute ischemic infarcts. The hypercapnic respiratory failure (pH 7.24, pCO2 70 mmHg) and refractory seizures that necessitated ventilation and several antiepileptics complicated the course. It took 6-10 weeks of intravenous ceftriaxone with serial CSF surveillance showing progressive response on day-28 CSF protein 159 mg/dL, WBC 153/cmm. Subsequent imaging showed that diffusion restriction was almost resolved with temporary subdural collections. There was an improvement in neurological status gradually and without focal deficits. NTS meningitis in immunocompromised infants can be the outcome of a nonspecific gastrointestinal disease and necessitates the early examination of CSF, neuroimaging, and long-term targeted treatment with close monitoring and evaluation for underlying immunodeficiency to minimize complications and the risk of relapse.
Keywords
Nontyphoidal Salmonella, Salmonella enterica, Meningitis, Infant, Bacterial Infections
Introduction
Nontyphoidal Salmonella (NTS) meningitis is an uncommon but severe invasive salmonellosis that causes infection in the meninges or the protective membranes of the brain and the spinal cord[1]. Salmonella species are facultative intracellular gram-negative bacilli in the family Enterobacteriaceae. NTS are serotypes that do not belong to Salmonella enterica serovars Typhi and Paratyphi, which are traditionally linked with enteric (typhoid) fever[2]. The NTS are most often involved in self-limited gastroenteritis; however, they may lead to bacteremia and focal invasive infections, such as meningitis, osteomyelitis, and endovascular infections in a minimal number of patients[3].
NTS meningitis typically affects susceptible groups, including neonates, young infants, and immunocompromised individuals[4]. Immunocompromise refers to a condition where the immune system lacks the capacity to provide an adequate response to pathogens, enabling organisms with low invasive potential to cause a systemic disease. The immature cell-mediated immunity, low gastric acidity, and underdeveloped blood-brain barrier (BBB) increase the risk of neonates, as the BBB promotes central nervous system (CNS) invasion[5]. Human immunodeficiency virus (HIV) infection, malignancy, diabetes mellitus (DM), chronic liver disease, or hemoglobinopathies, such as sickle cell disease, and immunosuppressive therapy, are predisposing factors in adults[6]. The pathogenesis of NTS meningitis includes initial colonisation of the gastrointestinal tract(GIT) after ingestion of contaminated food or water, such as poultry, eggs, or dairy products[7]. Salmonella is capable of surviving and replicating in macrophages after translocation through the intestinal epithelium, causing bacteremia. Hematogenous spread gives the organism access to the BBB, which is a selectively permeable interface, protecting the CNS against circulating pathogens. Salmonella causes an acute inflammatory reaction once in the subarachnoid space, leading to the development of meningitis that is characterized as inflammation of the leptomeninges and cerebrospinal fluid (CSF)[8].
Additionally, NTS meningitis clinically exhibits nonspecific characteristics, typically in neonates and infants. The typical clinical manifestations include: fever, irritability, poor feeding, lethargy, vomiting, seizures, and bulging fontanelle[9]. Classical signs of meningitis, which include photophobia, stiffening of the neck, and altered mental status, may be noted in older children and adults. Seizures are dominant in NTS meningitis, indicating direct CNS invasion and indirect complications such as cerebral edema or infarction[10]. NTS meningitis is linked to a more threatening onset and a greater neurological complication rate than meningitis. On the contrary, meningitis is caused by more common organisms, including Streptococcus pneumoniae or Neisseria meningitidis[11].
Diagnosis is made by isolating Salmonella species in CSF collected through lumbar puncture, sampling the CSF at the subarachnoid space[12]. The CSF usually indicates pleocytosis, which is an elevated count of white blood cells (WBCs), most of which are neutrophils, high levels of proteins, and low levels of glucose as compared to blood glucose. The blood cultures are often positive, which indicates simultaneous bacteremia[13]. Neuroimaging, such as computed tomography(CT) or magnetic resonance imaging (MRI), may be necessary to diagnose complications such as hydrocephalus[14]. It refers to excessive CSF in the ventricles, subdural empyema, which is characterized by pus between the dura mater and the arachnoid. In addition, cerebral abscess or infarction may also need neuroimaging[15].
The existing studies on NTS meningitis lack the detailed characterization of clinical presentation patterns and valid diagnostic criteria. Systematic data on the best antimicrobial therapy, such as CSF-penetrating, and treatment period are scarce. There is a paucity of evidence regarding the antibiotic resistance of CNS infection, and there is no standardized outcome measure or practical case series to guide prognosis or risk of relapse.
This case report aimed to represent a rare case of NTS meningitis, underscoring its clinical presentation, diagnostic challenges, and progression of the disease. Additionally, the case report fills the gap in the existing literature on this rare condition and enhances clinical awareness of its possible occurrence outside the typical gastrointestinal symptoms.
Case Report
Patient Information
A 4-month-old female patient of Middle Eastern descent was presented to the pediatric intensive care unit (PICU) with a 5-day history of fever, diarrhea, irritability, excessive crying, poor feeding, reduced activity, and lethargy. Following the symptoms, a day later, she was taken to another hospital and managed as acute gastroenteritis using intravenous (IV) cefotaxime and fluids. In the following two days, she experienced progressive prostration, irritability, and lethargy. A Computed Tomography scan (CT scan) of the brain before the referral was routine, and the patient was transferred to the PICU. She was delivered full term using cesarean section, birth weight 3000 g, with no unresolved neonatal history. She was breastfed and bottle-fed in the fourth month and regularly vaccinated for 2 months. No chronic illness history, past hospitalization, hereditary disease, or major family or psychosocial problems. The past treatment of this illness demanded IV cefotaxime without improvement. Despite the absence of any chronic conditions, the intensity and invasiveness of the infection raised a concern of an underlying immune defect. An immunological test was hence scheduled after stabilization.
Clinical Findings
When admitted to the PICU, the patient appeared sick, unresponsive, and irritated. Vitals revealed 151/min pulse, 42/min respirations, 85/45 mmHg blood pressure, 2s capillary refill, 98% oxygen saturation on room air, temperature 38°C. Anthropometry Weight showed 7 kg (49th percentile), length 66 cm (74th percentile), head circumference 42 cm (44th HC percentile), body surface area 0.36 m 2, surface area index 16.1, BMI percentile 30.35, and Glasgow Coma Scale was 13/15 neurologically. Both pupils were unequal yet responsive. The anterior fontanelle had levelled with augmented deep tendon reflexes. Clear conjunctivae and no stiffening of the neck, seizures, or ataxia were reported. Investigations revealed routine cardiovascular and respiratory investigations. The abdomen was slightly distended, and bowel sounds were audible.
Diagnostic Assessment
Baseline labs revealed WBC 12/uL, 42% neutrophils, 47% lymphocytes, hematocrit 25%, platelets 86, CRP 305mg/dl, procalcitonin 35.50ug/L, PT 13s, INR 1.3, D-dimer 2.9, as shown in Figure 1, Figure 2, Figure 3, and Figure 4. Liver enzymes, electrolytes, calcium, magnesium, and albumin, and renal profile were normal. First CSF analysis reported 247 mg/dl, protein, 0.38 mmol/L, glucose, 340/cmm. WBC, 230/cmm, Gram stain of both peripheral and central blood cultures demonstrated gram-negative rods, CSF, and gastrointestinal molecular panel all tested positive with ampicillin, cefepime, amikacin, ciprofloxacin, ceftriaxone, and meropenem sensitive Salmonella nontyphoidal. Urine analysis was not remarkable.
The MRI brain revealed several rim-enhancing T2 hyperintense and T1 hypointense lesions in the bilateral centrum semiovale and corona radiata, more on the left. These regions were accompanied by vasogenic edema and areas of limited diffusion indicative of cytotoxic edema, vasculitis, and acute ischemic white-matter infarcts. There was diffuse bifrontal leptomeningeal enhancement as shown in Figure 5.
Electroencephalogram (EEG) revealed left-sided burst-suppressed discharges of spikes and waves, sporadic right frontotemporal discharges, and generalized slowing, which are typical of acute epileptic encephalopathy. Echocardiography showed that there was a minor atrial septal defect of 3-4 mm.
Day-14 CSF revealed protein 600mg/dL, glucose 4.46mmol/L, WBC 200/cmm (30% neutrophils, 40% lymphocytes, 30% monocytes), RBC 42/cmm; culture negative, panel negative as illustrated in Table 2.
Day 28 CSF revealed RBC 36/uL, WBC 153/uL (1% neutrophils, 90% lymphocytes, 20% monocytes), glucose 4.9 mmol/L, protein 159mg/dl as shown in Figures 6, 7, 8, and Figure 9.
Final diagnosis was nontyphoidal Salmonella meningitis with meningoencephalitis, vasculitis, and secondary ischemic brain injury.
Therapeutic Intervention
Vancomycin and meropenem empirical IV were initiated. On Day 3, she yielded to acute hypercapnic respiratory failure necessitating intubation, mechanical ventilation, and a left internal jugular central line (pH 7.24, pCO2 70 mmHg). X-ray chest revealed right upper lobe consolidation as shown in Figure 10. Vancomycin was also used in the case of aspiration pneumonia and was discontinued at day 7 when cultures were negative.
Constant generalized seizures were treated by high-dose midazolam infusion, levetiracetam, phenytoin, and phenobarbitone. Neurosurgery stated not to have any ICP observations because the head circumference and fontanelle were at the same level, with the addition of dexamethasone in case of cytotoxic edema. The recommendation of de-escalation of meropenem to ceftriaxone and assessment of immunodeficiency after stabilization was advised in the case of infectious diseases. Ceftriaxone was administered over a period of 6 weeks with 4 weeks of extension because of continued irregularities. An immunological workup was later conducted, which confirmed the existence of an underlying immune disorder. The results proved the presence of the impaired host defense system, which predisposes the patient to the invasion by nontyphoidal Salmonella. This defective immune system is probably the cause of the severe clinical progression and vast involvement of the central nervous system.
Follow-up and Outcomes
On Day 9, she was extubated to a high-flow nasal cannula followed by room air. Follow-up EEG revealed generalized slowing of the EEG without epileptiform activity. Phenytoin and phenobarbitone could be gradually discontinued without a recurrence of seizures. MRI at 22-28 days showed that restricted diffusion had nearly resolved, and the rim-enhancing lesion had significantly declined with mild persistent leptomeningeal enhancement, as shown in Figure 11
Auditory and ophthalmologic brainstem response testing had normal results. A week after discharge, the patient had poor head control (since early illness) but no focal impairments, cranial nerve palsies, or meningeal findings.
MRI findings after five weeks showed bilateral loculated subdural collections of CSF-intensity/hygromas (largest 4 x 0.9 cm left frontal), smooth leptomeningeal enhancement, and small nodules of enhancement. It was recommended to continue using antibiotics. Another MRI revealed a new thin diffusion-restricting layer in the right parietal convexity, which indicated the possibility of a thin subdural abscess, ongoing leptomeningeal enhancement, slight shrinkage of earlier collections, and unchanged ventricular dilatation, as shown in Figure 7
After three weeks, the patient exhibited better head control, limb movement against gravity, head-circumference centiles, a mildly full anterior fontanelle, and no focal neurological deficits, cranial nerve palsies, or meningeal variations.
Discussion
NTS meningitis is a leading cause of morbidity and mortality, even with proper antimicrobial treatment. Mortality rates are very high compared to other bacterial meningitides, and survivors often develop long-term neurological sequela[16]. They are developmental delay, cognitive impairment, epilepsy, hearing loss, and motor deficiencies[17].
NTS meningitis is an uncommon, however fatal form of invasive salmonellosis in infants, which is marked by severe inflammation of the CNS and a large number of neurological complications[18]. Although antimicrobial therapy is used appropriately, the results are unpredictable, and the treatment should be prolonged with close neuroimaging monitoring. The current case report revealed that a 4-month-old infant with an underlying immune disorder may present with nontyphoidal Salmonella meningitis, which may progress rapidly with neurological impairment despite early antibiotic exposure, suggesting the invasive and destructive nature of the pathogen in susceptible hosts. In the present case scenario, a significant inflammatory response (CRP 305 mg/dL, procalcitonin 35.5 ug/L), severe cerebrospinal fluid (CSF WBC 340 cells/mm3, glucose 0.38 mmol/L, protein 247 mg/dL), and early neuroimaging (ischemic white-matter) injury were all indicative of aggressive CNS involvement. These findings are consistent with the study by Yilmaz et.al (2024), which also reported early ischemic alterations due to Salmonella-induced vasculitis and thrombosis in a newborn, which supports the vascular tropism of invasive Salmonella infections [19].
Contrary to the ordinary bacterial meningitis, the current case showed multifocal rim-enhancing lesions, cytotoxic edema, and diffuse leptomeningeal enhancement on MRI, which indicated combined meningoencephalitis and vasculitis. Similar neuroimaging findings were also observed in another case report by Al Haddabi et.al (2024), in which several supratentorial and infratentorial infarcts were associated with inflammation of small cerebral arteries. However, whereas the patient in Al-Haddabi's study went on to develop hydrocephalus, empyema, and long-term neurological outcomes, including hemiplegia and visual impairment, the current case report showed a gradual radiological resolution with long-term antimicrobial treatment, suggesting that early diagnosis and long-term therapy can alter the course of the disease[20].
The long-standing presence of CSF abnormalities in the present case is also a strong indication of the relapsing and refractory nature of NTS meningitis. By day 14, CSF protein was highest at 600mg/dL, and by day 28, it was still high (159mg/dL) even after sterile cultures. This biochemical persistence is similar to the case report by Palyvou et.al (2025), which showed that ventricular dilatation and subdural collections developed later in the course of the disease, and extended intravenous antibiotic therapy was required for five weeks.
The complications were mainly pressure-induced, whereas the case in point exhibited ischemic injury and epileptic encephalopathy, which was proved by EEG results of burst suppression and generalized slowing, indicating a more widespread parenchymal involvement.
Another essential characteristic was seizure activity. The present case progressed to intractable seizures that needed more than one antiepileptic agent, which was in line with the past case reports, where focal seizures were the most common symptoms of cerebral ischemia[19, 20]. It is noteworthy that the current case had a successful seizure control and eventual EEG normalization, but the case report by Al Haddabi et.al (2024) had persistent focal seizures at 12-month follow-up, which means that the neurological outcomes are heterogeneous despite similar radiological insults[20].
In contrast to the case report by Borger et.al (2025), which described a fatal outcome in a 27-week-old premature baby with Salmonella sepsis and meningitis, the current case was referred to a baby with no known immunodeficiency, which indicates that host maturity and timely intensive care play a significant role in survival. Although the study was dedicated to maternal transmission and devastating systemic infection, the present case report explains gastrointestinal entry and subsequent hematogenous spread, which supports several pathogenic pathways of invasive NTS disease[21]. Notably, invasive nontyphoidal Salmonella infections are common among immunodeficient patients. Malfunctions of cell-mediated immunity, dysfunctions of macrophages, defects in complement, or malfunctions in humoral immunity are major risk factors of bacteremia and intrusion of the central nervous system[22]. The diagnosis of an immune disorder in the current case is a crucial component explaining the depth of meningoencephalitis, vasculitis, ischemic injury, and persistent seizures. This indicates the fact that NTS meningitis during the first infancy years should be followed by intensive immunological investigation, especially in case of a rapid or complex course of the disease.
Even though the study conducted by Penfold et.al (2025) reported invasive NTS, which presents as osteomyelitis and pyomyositis as opposed to meningitis, it supports the ability of Salmonella enterica to induce deep-seated focal infections that need extended antibiotic treatment of about 4-6 weeks. This is similar to the six-week course of ceftriaxone required in the present case to provide clinical and radiological improvement, which justifies the prolonged treatment in invasive NTS infections[23].
Altogether, the present case report has shown that NTS meningitis is not a simple acute infection but a dynamic inflammatory and vascular disease with changing complications. In comparison to the available reports, it supports the need to conduct early MRI, serial CSF testing, vigorous seizure control, and extended antimicrobial treatment to reduce the long-term neurological harm [13, 19, 23, 24].
Strengths and Limitations
The key strength of the case report is its longitudinal assessment, with serial CSF analyses, sophisticated neuroimaging, and electrophysiological monitoring, which offers a thorough evaluation of the development of the disease and the response to treatment. Another successful neurological recovery with such extensive ischemic injury is also reported, which provides valuable outcome data to the limited literature. Also, the fact that an underlying immune disorder was identified enhances the clinical relevance of this case report and the need to perform the assessment of the immune system in infants with invasive Salmonella infections. The major weakness is that it has a single-case design, which limits generalizability.
Conclusion
Nontyphoidal Salmonella in infants may result in severe meningoencephalitis, vasculitis, ischemic brain damage, and refractory seizures despite early antimicrobial exposure. It underlines the significance of early neuroimaging, long-term use of intravenous antibiotics, and close neurological follow-up. This case also highlights the need to assess underlying immunodeficiency in infants with invasive nontyphoidal Salmonella meningitis since immune dysfunction can play a very significant role in determining the severity and outcomes of the disease. Early intensive care and personalized treatment can be of great benefit to the survival and neurological outcome in this disease.
Statements and Declarations
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References