Nosocomial Infections (NCIs) or Hospital Acquired Infections (HAIs) are the leading cause of public health issues worldwide with variation in prevalence rates (26). The main strategies for managing these infections are the source and understanding of the conditions, the pathogens involved in HAI, and its risk factors (27).
The majority of the ICU patients experiences nosocomial bloodstream infections, total leukocytes count (TLC) and C-reactive protein (CRP) play a pivotal rule in the diagnosis of these infections (28–31). The current study observed that 60% of the nosocomial patients have leukocytosis that describes the possible important role of leukocytosis in nosocomial infection, as describes earlier (28–31). Lymphopenia and risk of infection are poorly studied; however, according to a report, there is a 2.4-fold increased risk of lower respiratory tract infection and urinary tract infection with lymphopenia (32). So for another study at ICU reports that lymphopenia at admittance was associated with a 1.6-fold increased risk of infection(33). Similarly, in the general population, lymphopenia was associated with an increased risk of hospitalization due to conditions like sepsis, endocarditis, diarrheal disease, pneumonia, urinary tract infection, and skin infection (34). In the literature (35–37), it is well established that, in many cases, febrile neutropenic patients have bacteremia without any specific focus (37). Although most infections of neutropenic patients' are only clinically documented (37–39). The above-mentioned reports assist our current study, where we found 73.3% of the nosocomial patients with lymphopenia. However, discrepancies between the findings in the present and former studies (32, 40, 41) may be due to our study design that includes only nosocomial patients. The current study found Neutrocytosis in 73.3% of nosocomial infected patients as Neutrocytosis is frequently observed in the circulation and tissues during bacterial or fungal infections (42). The Neutrocytosis in the current study may be due to their important role during fungal and extracellular bacterial infections where they promote bacterial clearance through phagocytosis, production of reactive oxygen and nitrogen species (ROS/RNS), neutrophil extracellular trap (NET) formation, and production of pro-inflammatory cytokin(43, 44).
According to the current study, 33.3% of the nosocomial patients have thrombocytopenia, 12% have abnormal PT. In comparison, 8% have abnormal APTT; likewise, prolonged PT of 63.3% was observed in neonatal septicemia during nosocomial infection, more frequently among gram-negative infected patients (45). The deviation of our results may be because of different pathogenic microbes in the study may complicate infections by consumption coagulopathy (46), as well as the difference in the exposure to endotoxins, which may be attributed to the direct action of the endotoxins on endothelial cells or maybe an indirect result of the production of interleukin1 or tumor necrosis factor (47, 48).
The liver is one of the vital organs exposed to both hepatotropic and non-hepatotropic viruses and bacteria through the portal and systemic circulation and causes liver injury, either direct invasion or indirect cytokines and toxin production (49, 50). However, patients of Pneumococcal pneumonia and lobar pneumonia caused by one of the bacteria among S. pneumonia, P. aeruginosa, S. aureus, or Haemophilus influenza sometimes show elevated concentrations of bilirubin and Serum glutamic pyruvic transaminase/serum aminotransferases (SGPT/ALT) (51). Similar reports of elevated ALT/SGPT and bilirubin have been reported in typhoid fever caused by Salmonella typhi and gastroenteritis caused by nontyphoidal Salmonella (most commonly S. enteritidis and S. Typhimurium) (52). Consistently in the current study, an elevated level of SGPT/ALT, Bilirubin, and ALP among 60%, 26.7%, and 13.3% were found respectively among nosocomial patients. The changes in liver function tests in case of nosocomial infection are may be due to hepatic injury caused by nosocomial pathogens. So for in case of liver dysfunction during systemic disease, proper microbial examination, and sufficient knowledge about non-hepatotropic agents are necessary (49).
The said study finds that among nosocomial patients, 33.3% have an abnormal level of Urea. In comparison, 46.7% have an uncommon level of Creatinine; however, to our knowledge, there are no data to suggest whether or not the association of renal function test and nosocomial infection. Some previous studies report the higher risk of disease caused by MDROs, MRSA and VRE, in patients undergoing hemodialysis (53, 54). The renal function test increase may be due to the kidneys complication, either direct kidney injuries or immune-mediated injuries caused by all viruses, bacteria, mycobacteria, fungus, and protozoa (55) founds in nosocomial infections.
The current study reports that upon electrolytes analysis of nosocomial patients, 26.7% have Hypernatremia, 20% have hyperchloremia, while 6.7% have Hypokalemia. The change in various electrolytes might be due to the excessive use of antibiotics, which are directly proportional to NIs. Their adverse effects may be responsible for electrolyte abnormalities such as aminoglycosides, amphotericin B, trimethoprim, and tetracycline cause electrolyte disturbance (56–58).
The prevalence of culture-confirmed nosocomial infection in the current study was 25%, which is lower than other reports of 29.13% by Shaikh et al. (59), 27.03% by Noor et al.(60) from Pakistan, 35.8% from Ethiopia (61), however higher than that of Rabat, Morocco (10.3%) by (62), 6.9% in Eastern Ethiopia by (26), 0.3% from ambarene, Gabon by (63), and 1.03% from Mazandaran, India (64). The results may be due to many factors, like the difference in patient selection criteria, the case mix, ICU type, length of stay, device utilization rate, and discharge criteria (65, 66). The current study shows that the ratio of gram-negative vs. gram-positive isolates was 83.3%:16.6%, similar to other studies that most nosocomial infections occurring in the ICU are due to Gram-negative bacteria (19, 67). The precise pattern of causative organisms, whether bacterial or fungal, varies across countries and between ICUs according to patient case mix, infection site, antibiotic protocols, infection control practice, and local ecology and resistance patterns (28).
The current study shows that SSI contributes 13.3% of all infections, which was higher compared to the survey from Ethiopia (10.9%) (68), Iran (8.6%) (69) while lower as compared to (31.5%) reported by Tolera et al.(26). The prevalence of BSIs (26.6%) in this study was relatively comparable with the findings of (22.7%) by Shaikh et al. (59) from Pakistan and Ethiopia (20.8%) (61) while much higher compared with the study performed at Bahirdar (2.4%) (68). The current study reported 36.6% of the nosocomial infection was UTI which is higher than 9 .03% and 9.4% reported by (70, 71) respectively. The discrepancy in the results may be due to the difference in the frequency of NSI in various developed and developing countries (72).
The current study found that the most frequent bacteria causing NIs were K. pneumonia (40%) and S. aureus (16.6%), consistent with other findings (61, 64, 73). The current study shows that imipenem was the most effective antibiotic against gram-negative isolates of Klebsiella pneumonia, K. oxytoca, Proteus spp, Serratia liquefaciens Serratia marcescens. Simultaneously, the majority of the resistance was found against Amoxicillin + Clavulanic acid, Trimethoprim/sulfamethoxazole, cefoxitin, Levofloxacin, Norfloxacin, and linezolid. Similar supporting results of sensitivity for Klebsiella pneumonia and Klebsiella oxytoca were reported (74–76). According to a study, K.pneumoniae was found resistant to all β-lactams and meropenem however susceptible to imipenem by (77) and resistance to all ß-lactams, including meropenem except imipenem was found by (78–80). A similar consistent result of sensitivity against Proteus spp was found elsewhere (81, 82). Meropenem and imipenem were the potent antimicrobials against Proteus spp. (83, 84), in contrast to the resistance against imipenem and aztreonam by (85). Resistance rates were noted highest against ceftriaxone, ceftazidime, and piperacillin/tazobactam (86). According to a study, the isolated Serratia strain was sensitive towards imipenem, cefotetan, gentamicin, etc. (87), supporting the reported result of susceptibility to imipenem, meropenem, and amikacin, etc. (88). The sensitivity of S. marcescens was detected for imipenem, meropenem, and ceftazidime, etc. (89). The resistance of S. marcescens towards fluoroquinolones and third-generation cephalosporins was found by (88, 90–97).
Methicillin-Resistant Staphylococcus aureus (MRSA) was the only gram-positive isolate found in the study, highly sensitive towards Trimethoprim/sulfamethoxazole while resistant towards linezolid, Imipenem, and Cefotaxime, etc. Consistently similar reports from various countries show that around 90% of S. aureus isolated from nosocomial infections and community remain sensitive to Trimethoprim/sulfamethoxazole from the USA (98–100), Europe, Israel, and Turkey (101–103), Japan (104), Canada (105–108). A study reports higher susceptibility to amoxicillin + clavulanic acid, Doxycycline and Gentamicin, etc. (109). In contrast to the above reports, 30% of hospital-acquired MRSA in Australia, 19% in sub-Saharan Africa (110), and 85% from India (111, 112) were resistant towards Trimethoprim/sulfamethoxazole. Various reports observed resistance of s.aureus towards ampicillin and penicillin, rifampicin and clindamycin, oxacillin and erythromycin (108), Azithromycin, Ceftriaxone, Cefixime and Penicillin (109), Gentamycin, Erythromycin, Levofloxacin and Tetracycline (113). The divergence in the findings could be attributed to the mechanism of resistance like the permeability barrier, efflux pumps, mutational or recombinational changes in the target enzymes and acquired resistance by drug-resistant target enzymes in various antibiotics and alteration of the target with decreased affinity for the antibiotics (114).