C. violaceum is a tropical pathogen that rarely affects humans. its fatal infectivity in buffaloes was first described by Woolley in 1905 [3] ; Lessar JE reported the first human case in Malaysia in 1927 [3], and nearly 200 human cases have been reported in the English literature. The English literature was searched in PubMed, Web of Science and other online databases using the search terms " C. violaceum, infant, child, neonate” for the time period between 2015 and June 2024 only. Data were comprehensively collected and duplicates removed. A total of 16 case series of childhood infections were collected (excluding these cases), most of which were case reports (Table 1). Most cases of childhood infections were from tropical and subtropical regions. C. violaceum have been reported to be predominantly found in warm climates between 35°N latitude in the north and south of the world [3]. The patients in cases 1 and 2 of this paper were from southern China distributed in coastal areas with high summer temperatures (about 30 °C). The source of infection was mostly community-acquired, with 62.5% of the children suspected to have been exposed to the organism through damaged skin, and 37.5% had a clear history of water or soil exposure. As in previous studies, children with skin damage and exposure to contaminated water or soil were predisposing factors. Occasional cases of hospital-acquired infections have been reported [4]. Immunodeficiencies such as CGD, diabetes mellitus, and glucose-6-phosphate dehydrogenase (G6PD) deficiency may be important susceptibility factors [2]. In these situations, neutrophils and monocytes lack the ability to produce the oxygen metabolites required to kill phagocytosed bacteria, which makes patients more susceptible to develop sepsis and for the infection to spread to various visceral organs [14]. In this article, no underlying predisposing diseases were found in either of the two pediatric patients. Among the infected children, majority were boys (62.5%) and minority were girls (37.5%). The possible reason for the gender difference was that most boys were more active and participated in more outdoor activities than girls. They are more exposed to stagnant water, soil and injuries than girls.
Table 1 Children infected with C. violaceum reported in the English-language literature from 2015 to 2024Clinical signs of C. violaceum infections are varied. Most infections follow exposure through the skin and mucous membranes, causing localised skin infections, sepsis and visceral abscesses (mainly in the liver and lungs), while other clinical manifestations may include urinary tract infections, osteomyelitis, fasciitis, ocular infections, meningitis, otitis media, and may even lead to serious conditions such as haemophagocytic syndrome, respiratory distress syndromes, and multi-organ dysfunction. Of the seven children with serious conditions (serious illness defined as survival or death in the intensive care unit(ICU)), all had sepsis. Therefore, in children, sepsis is a significant predictor of poor outcome and death. The children in our case had sepsis. Previous studies have shown the mechanism of injury of C. violaceum, the bacteria can invade by damaging the host’s epithelial cells and also promote abscess production through metalloproteinases (MMP-2), as well as virulence mechanisms such as the quorum-sensing system (CviI/CviR) and the bacterial III secretion system (T3SS) [5]. A review of the literature showed that the mortality rate of children infected with C. violaceum in the last decade was 18.75%, which is much lower than the 53% mortality rate reported previously [6]. There may be increasing recognition of the virulence of C. violaceum, and increased positivity of cultures, more aggressive and effective antibiotic therapy, and more advanced adjunctive therapies (extracorporeal membrane oxygenation (ECMO), continuous renal replacement therapy, mechanical ventilation, etc.) may help to reduce mortality. Of the seven children with severe disease who survived, 100 per cent had varying degrees of use of advanced adjuvant therapies.
The diagnosis of C. violaceum infection must take into account the patient’s history of exposure, clinical presentation, and exclusion of colonisation, based on blood or pus culture results. When pediatric patients present with severe conditions such as sepsis symptoms, NGS can be selected to assist in diagnosis. NGS is a very promising tool for rapid diagnosis of Clostridium difficile infection, which can prevent delayed diagnosis and misdiagnosis of Clostridium difficile infection in patients with purulent discharge and negative blood culture tests [7]. Regarding treatment, are no clear guidelines for diagnosis and treatment. C. violaceum are usually resistant to penicillin, first- and second-generation cephalosporins, with variable susceptibility to third-generation cephalosporins, carbapenems andaminoglycosides [8]. Ciprofloxacin has been shown to be the most effective antibiotic against purple chromobacteria, followed by norfloxacin and parfloxacin [5]. Limited data suggest that the mechanism of resistance may be related to the production of β-lactamases and modification of lipid A to β-lactams and polymyxins within this bacterium [2]. Same as drug susceptibility in children. Out of 16 cases recorded, 10 (62.5%) children were treated with ciprofloxacin or other quinolones with good efficacy and prognosis. When treating children with C. violaceum infections, the recommended medication is ciprofloxacin if the child is severely ill, and medications with relatively few side effects for children, such as gentamicin, cotrimoxazole, and imipenem, can be chosen if the child has a non-severe illness. However, in paediatric patients, quinolones may lead to a risk of irreversible bone and joint damage [9]. For therapeutic medications, ingredients such as palmitic acid, theophylline, and taurine need to be further studied for effective treatment of the disease [9]. In previous studies, severely ill patients with immunodeficiency required antibiotics for at least 6 weeks, while some reports suggest that treatment may last up to 3 month [6]. Antibiotics may be used for several months depending on the therapeutic needs to reduce the risk of disease recurrence. A shorter duration of treatment may be appropriate in cases of mild infection. There is no evidence of a specific duration of treatment, but follow-up is recommended. All two children described here were very ill. In Case 1, antibiotics was given for more than 6 weeks. The child recovered completely.
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