This was the first study on the bacteriological profile of SBP in Madagascar. This study was essential because it had made it possible to establish the bacteriological and clinical profile of SBP in Malagasy patients with cirrhosis. This study had limitations. This is a single-center study and limited to those of inpatients. In-hospital prevalence of SBP was 25.58%, which corresponded to data from Western literatures (10-30%) [1, 2, 7]. Duah et al (Ghana, 2019) found a prevalence of 25.24%, similar to our study [8]. While, Oladimeji et al (Nigeria, 2013) reported a very high in-hospital prevalence at 67.7% [9]. These results are explained by the low number of the cirrhotic population during the study period, a high rate of culture positive (66.7%). Abdominal pain, fever and diarrhea were the most common symptoms during SBP. This finding has been reported by many authors (Setoyama et al; Shi et al) [10, 11]. The presence of these symptoms should alarm the clinician, suggesting the introduction of a probabilistic antibiotic therapy, without waiting for the results of the samples. Despite the low prevalence of hepatic encephalopathy in our series (6.06%), many studies reported a high rate of it during SBP [10, 11]. The presence of hepatic encephalopathy should systematically seek an SBP. Bacterial translocation is increased in gastrointestinal bleeding in patients with cirrhosis. Gastrointestinal bleeding was a risk factor to SBP [12-15]. Primary prevention of SBP with prophylactic antimicrobials should be initiated in gastrointestinal bleeding in patients with cirrhosis [2, 16-18]. In our study, gastrointestinal bleeding was present in only 6 patients (18.18%) with SBP.
In recent years, many authors have reported an upsurge in nosocomial SBP [11, 19-21]. Shi et al (2017) found a nosocomial SBP rate of 44.9% [11]. Ning et al (2018) reported nosocomial SBP in 47.8% of patients [18]. Other previous studies (Campillo et al in 2002; Cheong et al in 2009) also had high rates of nosocomial SBP [20, 21]. Contrary to published data, the nosocomial SBP rate was low (12.12%) in this present study. These high rates of nosocomial SBP could be explained in part by the fact that the patients included in these studies had frequent previous hospitalizations and had long hospital stays. In this study, community-acquired SBP occupied the majority of cases (87.88%).
In patients hospitalized with decompensated cirrhosis, 6.06% had bacterascites. This was comparable to the data in the literature (11%) [2, 16]. It could be due to transient colonization of ascitic fluid, or to an early phase of SBP [16]. Bacterascites should be considered an SBP in the presence of suggestive clinical symptoms, requiring antibiotic therapy from the outset. According to the literature, 20 to 30% of cultures performed were negative [2, 16, 17, 22]. They are higher (72.73%) in this study. The absence of the pathogen, although frequently found, does not eliminate SBP [16, 23]. Only 27.27% of the patients in our series had a positive culture. These results were comparable to those of Xiao et al (South Korea) [24] and Sanjaya et al (United States) [25] with a respective rate of 21.49% and 20%. Among the positive cultures, the majority of the bacteria found were Gram negative bacteria (66.67%). The other authors observed similar results: Oladimeji et al (Nigeria, 68.1%) [9], Attia et al (Cote d'Ivoire, 70%) [7], Piroth et al (France, 66%) [ 3], Shi et al (China, 50.6%) [11], Cheong et al (South Korea, 57.2%) [21], Reginato et al (Brazil, 57.4%) [26].
This is explained by the characteristic of digestive pathogens, of which Gram-negative bacteria are predominant. Escherichia coli (44.44%), Streptococcus mitis (33.33%), Klebsiella (11.11%) and Pseudomonas (11.11%) were the pathogens identified. This confirms those that have already been described; Dever et al (United States) [23], de Attia et al (Cote d'Ivoire) [7], Duah et al (Ghana) [8, 12] and Mohamed et al (Egypt) [27]. Since SBP's mechanism in cirrhotics is bacterial translocation, this explains these findings. The recommendations on treatment of SBP targeting Gram-negative bacteria as first-line may therefore be applicable. Two cases of Escherichia coli resistant to antibiotics were identified, including one case of resistance to cephalosporins and one case to sulfamethoxazole/trimethoprim. Kirplani et al (Pakistan) [28] found cases of Escherichia coli resistant to Ceftriaxone (32%) and Sulfamethoxazole/trimethoprim (10.9%). Another study by Ding et al showed similar results [14]. The frequent and inadequate use of cephalosporins and sulfamethoxazole/trimethoprim in Madagascar may explain these facts [29]. The use of quinolones and amoxicillin-clavulanic acid are suitable alternatives in this case. Pseudomonas was resistant to cephalosporin and Sulfamethoxazole/Trimethoprim. It was most often a nosocomial germ and also had a natural resistance to certain antibiotics including cephalosporin, nalidixic acid, Fosfomycin, sulfonamides [30]. A case of nosocomial infection with Klebsiella has been identified. He was multidrug resistant and was only susceptible to Amikacin. Several authors (Nousbaum et al and Ariza et al) reported that 25% to 50% of germs during nosocomial SBP were resistant to the usual antibiotics [2, 16, 31]. This reiterates the need for a systematic performance of a bacteriological examination with antibiogram in the face of any suspicion of an SBP.
Indeed, clinicians must be vigilant in the face of the emergence of multidrug-resistant pathogens. Current recommendations called for the use of Cefotaxime (2g/8h) for 5 days, either amoxicillin/clavulanic acid (1g/8h) for 7 days, or Ofloxacin (400mg/day) for 7 days, in case of community-acquired SBP. Piperacillin/tazobactam or Carbapenem are recommended in case of nosocomial SBP. The initial antimicrobials will be adapted according to the antibiogram [16, 32, 33]. In this study, quinolones were the most used, probabilistically, (57.58%) with a mean duration of 7 ± 2.98 days (Extreme: 2 to 14 days). Given the high prevalence of Gram-negative bacteria found in this study, the initial antimicrobial with quinolones was well suited.
The effectiveness of antibiotic therapy is defined according to the International Ascites Club as a decrease of at least 25% in the level of PMN in ascites after 48 h of treatment [2, 16]. This effectiveness will dictate the duration of treatment, explaining the variation in the duration of antibiotic therapy in this study.
In-hospital mortality rate was 15.15%. The deceased patients all had positive cultures. It was comparable compared to some studies (10 to 50%) [2-6, 16, 21, 34-37], while it was lower compared to the others studies: Heo et al (21.9%) [34] , Oliveira et al (41%) [35], Tandon and Garcia-Tsao (29%) [4], Poca et al (28%) [36, 37], Follo et al (24%) [38] and Cheong et al (49%) [21]. The difference in the findings can be explained, on the one hand, by the difference between the study populations; on the other hand, the multitude of management structures. However, SBP remains an absolute medical emergency, with a poor prognosis. The speed of the diagnosis of SBP, the susceptibility of pathogens to probabilistic antimicrobials as well as the precocity of the treatment can be key elements for the success of the management of SBP.