The present study showed that infection commonly complicates acute phase after stroke. In our study, 32 patients developed infection in the acute phase post-stroke which implies to an infection rate of 32%. This rate was similar to the infection rate reported in the meta-analysis by Westendorp et al. (2011). By comparing this rate of infection occurring post-stroke to the average rate of nosocomial infections in our hospital (5%), we found that stroke significantly increased the rate of nosocomial infections. This was in agreement with Meisel et al. (2005) who reported post-stroke infection rate ranging from 21 to 65%, while the average nosocomial infection rate was ranging from 6 to 9% in all hospitalized patients. We found that the most common infections were pneumonia (66% of infections and 21% of all patients), and the second most common was urinary tract infections (47% of infections and 15% of all patients). The other reported infections were blood infection and subcutaneous infection with markedly lower incidence rates (5% and 3% of all patients) respectively. And interestingly, no central nervous system (CNS) infection was recorded in any patient in our study. These results are similar to that reported by Westendorp et al. (2011), who also found pneumonia and UTI to be the 2 most common post-stroke infections. However, Westendorp et al. (2011), in his meta-analysis stated that there was a wide range of variations in the infection rate of pneumonia (1–33%) and urinary tract infections (UTI) (2–27%). On the other hand, Harms et al. (2011) found that UTI occurred more common than pneumonia with an infection rate ranging from 6 to 27%, while that of pneumonia was ranging from 5 to 22%. A very significant correlation was found between the severity of stroke as indicated by a higher NIHSS score and the development of infection (p value < 0.001). This is completely in agreement with Minnerup et al. (2010) who also found that higher NIHSS score was associated with all types of infections. We also found a significant correlation between the size of the infarction and the development of infection (p value < 0.001). In our study, lesion was divided according to the size: to small (< 1.5 cm), moderate (1.5–5 cm), and large infarctions (> 5.0 cm or > 1/3 of the MCA territory). In our study, a significant association was noticed between the occurrence of post-stroke neurological complications (brain edema, disturbed conscious level (DCL), and stroke recurrence) and the occurrence of infections. Interestingly, we also found a significant association between the rate of reduction in blood flow in carotid arteries elicited by carotid duplex and the development of infections. Aslanyan et al. (2004) also found that post-stroke infection rate was associated with the patients’ clinical condition. Studies including patients with a higher stroke severity or lower levels of consciousness showed higher infection rates, in particular for pneumonia. This effect corresponds with previous studies that often report both characteristics as risk factors for pneumonia. We found that patients who developed infections are significantly older in age (68.8 ± 10.2), with higher female predominance (34%), comparing to those who did not have stroke 57.8 ± 7.8 and 7% respectively. This was in agreement with Ovbiagele et al. (2006) who also found that advanced age was a risk factor for post-stroke infection. We also found a significant correlation between the occurrence of post-stroke infection and a positive history for stroke or transient ischemic attack or both of them with a p value of < 0.001 for each of them. On the contrary, no association could be found between infections and each of diabetes mellitus (DM), hypertension (HTN), and hyperlipidemia, IHD, or PVD. And interestingly, a significant correlation was found between the presence of atrial fibrillation and the development of post-stroke infection (p value = 0.001). We also found that, the best predictors of post-stroke infections are higher age > 61 years, higher NIHSS score > 9.5, infarction size that is larger than small and more severe carotid stenotic lesions causing > 27.5% flow reduction as elicited by duplex study. In our study, pneumonia was the commonest post-stroke infection occurring to 21 patients (21%). Risk factors significantly associated with post-stroke pneumonia were bulbar manifestations, Ryle insertion, age > 61, female gender, AF, NIHSS > 9.5, size of infarction larger than small and previous CVS or TIA. Westendorp et al. (2011) found that pneumonia is the most common post-stroke infection, and that most strokes related pneumonias are believed to result from dysphagia and subsequent aspiration of oropharyngeal material or gastric content. In our study, the commonest organisms responsible for post-stroke pneumonia were coagulase negative Staph (5 patients), methicillin resistant staphelococcus aureus (MRSA) (5 patients), Pseudomonas (4 patients), E-coli (4 patients), Acinetobacter (3 patients), Klebsiella (2 patients), and Candida (1 patient). Gram-negative bacteria and Staphylococcus aureus are known to cause pneumonia by aspiration of endogenous material from the colonized oropharynx (Millns et al. 2003). These pathogens are often seen in nosocomial infections. On the other hand, Streptococcus species is still the most detected pathogen in community acquired pneumonia (Jones 2010). Our results regarding the commonest pathogens were almost in agreement with Westendorp et al. (2011) who found that microbiologic data of patients with post-stroke pneumonia shows a pattern of mostly early onset nosocomial pneumonia, or a community acquired aspiration syndrome. Staphylococcus aureus and gram-negative bacteria such as Klebsiella pneumoniae, Pseudomonas aeruginosa, Escherichia coli, or Enterobacter were commonly identified, also Streptococcus species are occasionally found. Post-stroke pneumonia usually occurs within the first 3 to 5 days after hospitalization and thus can be considered as early-onset (HAP) hospital-acquired pneumonia (Schwarz et al. 2008). Harms et al. (2011) stated that early-onset HAP is primarily attributed to Gram-negative bacteria, such as Haemophilus influenzae, and Gram-positive bacteria such as methicillin (methicillin)-sensitive Staphylococcus aureus (MSSA) and S. pneumoniae, while late-onset nosocomial pneumonia is usually attributed to higher-level antibiotic-resistant Gram-negative bacteria (e.g., Pseudomonas aeruginosa, Acinetobacter spp.) and Gram-positive bacteria (e.g., MRSA). In our study, urinary tract infection was the second most common post-stroke infection that affected 15 of our patients (15%). The most important factor associated with post-stroke UTI was insertion of urinary catheter (p value < 0.001). Other significantly associated risk factors were female gender, old age, AF, NIHSS > 9.5, size of infarction larger than small, and previous CVS or TIA. Stott et al. (2009) similarly reported that a higher age and female sex were found to be significant risk factors for urinary tract infection. In our study, different pathogens isolated from urine cultures were E. coli (12 patients), Klebsiella (2 patients), Acinetobacter (1 patient), Proteus V. (1 patient), and candida (1 patient). Zhanel et al. (2005) found that the most common pathogen in UTI remains Escherichia coli (55–80%). In about 5–10% of cases, other Entero-bacteriaceae, such as Proteus mirabilis and Klebsiella spp., can be isolated, and occasionally, Staphylococcus saprophyticus is isolated.
