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Helicobacter Pylori Assay And Urine Bacteriology Of Patients With Gastritis

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INFECTIOUS DISEASE & MICROBIOLOGY

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ABSTRACT

Helicobacter pylori are a non-spore-forming Gram-negative bacterium. The cellular morphology may be curved, spiral, or fusiform, typically 0.5 to 1.0 μm in width and 2.5 to 5.0 μm long. The aim of this study is to determine and compare the prevalence of H. pylori infection and urinary tract infections among gastritis patients. The subjects used in this project work comprised of patients with gastritis. A total number of twenty-five (25) patients with gastritis were recruited for this study. The predominant isolates were Escherichia coli (4), Klebsiella spp (2), Enterobacter spp (2), Staphylococcus aureus (3), Streptococcus spp (3) and Proteus vulgaris (2) with Escherichia coli having the highest prevalence of 25%. The antibiotic susceptibility patterns of the various isolates were read using their zones of inhibitions on the sensitivity culture plates, which shows that Ciprofloxacin, Gentamycin, Streptomycin and Refampicin were the most sensitive antibiotics against the gram positive bacteria isolates (Streptococcus spp and Staphylococcus aureus) while other drugs were found to be intermediate and resistant. The gram negative organisms (Enterobacter spp, Escherichia coli, Klebsiella spp and Proteus vulgaris) were more sensitive to Augmentin and Gentamycin, while Ofloxacin, Peflacine, Ciprofloxacin, Septrin and Ampicillin were intermediate while the other drugs were resistant. The noninvasive test-and-treat strategy for H. pylori infection is reasonable for younger patients who have upper gastrointestinal symptoms but not alarm symptoms, like the patient in the vignette. Noninvasive testing can be performed with the use of the urea breath test, fecal antigen test, or serologic test; the serologic test is the least accurate

TABLE OF CONTENT

Cover page
Title page
Certification
Dedication
Acknowledgement
Table of Content
List of Plates
List of Tables
Abstract

Chapter One
1.0 Introduction 1
1.1 Background to the Study 1
1.2 Justification of Study 3
1.3 Research Questions 4
1.4 Research Hypothesis 5
1.5 Aim of Study 5
1.6 Specific Objectives of the Study 5

Chapter Two
2.0 Literature Review 6
2.1 Overview of Helicobacter pylori 6
2.2 Microbiology of H. pylori 7
2.3 Epidemiology of H. pylori 8
2.4 Symptoms of H. Pylori Infection 9
2.5 Effects of Helicobacter pylori on Gastric Physiology 10
2.6 Complications of H. pylori Infections 10
2.7 Gastritis and Gastric Cancer 11
2.8 Diagnostic Testing of H. pylori 12
2.9 Management of H. pylori 16
2.10 Urinary Tract Infections 18
2.11 Epidemiology of UTI 19
2.12 Signs and Symptoms of UTI 20
2.13 Causes of UTI 21
2.14 Diagnosis of UTI 23
2.15 Treatment of UTI 24

Chapter Three
3.0 Materials and Methods 25
3.1 Area of Study 25
3.2 Study Population 25
3.3 Research Design 25
3.4 Inclusion and Exclusion Criteria 25
3.5 Sample Collection 25
3.6 Sample Analysis 26
3.7 Antibiotic susceptibility testing 27
Chapter Four
4.0 Results 28

Chapter Five
5.0 Discussion, Conclusion and Recommendation 37
5.1 Discussion 37
5.2 Conclusion 40
5.3 Recommendation 40
References 42
Appendices 48

CHAPTER ONE

INTRODUCTION
1.1 Background of the Study
Helicobacter pylori are a non-spore-forming Gram-negative bacterium. The cellular morphology may be curved, spiral, or fusiform, typically 0.5 to 1.0 μm in width and 2.5 to 5.0 μm long. The spiral wavelength may vary with the age, growth conditions, and species identity of the cells. In old cultures or those exposed to air, cells may become coccoid (Shirai et al., 2000).
The genus Helicobacter belongs to the ε subdivision of the Proteobacteria, order Campylobacterales, family Helicobacteraceae. This family also includes the genera Wolinella, Flexispira, Sulfurimonas, Thiomicrospira, and Thiovulum. To date, the genus Helicobacter consists of over 20 recognized species, with many species awaiting formal recognition (Fox, 2002). Members of the genus Helicobacter are all microaerophilic organisms and in most cases are catalase and oxidase positive, and many but not all species are also urease positive. Helicobacter species can be subdivided into two major lineages, the gastric Helicobacter species and the enterohepatic (nongastric) Helicobacter species. Both groups demonstrate a high level of organ specificity, such that gastric helicobacters in general are unable to colonize the intestine or liver, and vice versa (Fox, 2002).
Currently, several direct diagnostic tests, including histopathology and/or immunohistochemistry (IHC), rapid urease test (RUT), and culture are frequently used as they provide genotype and antibiotic resistance information. However, due to the small amount of bacteria that colonizes the stomach, the direct test sensitivity decreases. Thus, several indirect tests, including antibody-based tests such as serology and urine test, urea breath test (UBT), and stool antigen test (SAT) have been developed to diagnose H. pylori infection (Burucoa et al., 2013).
Among the indirect tests, UBT is one of the most accurate to determine H. pylori infection with a sensitivity and specificity of 99% and 98%, respectively (Gisbert and Pajares, 2004). Together with SAT, UBT became the best method to identify active infection, which cannot be detected by serology (Malfertheiner et al., 2012).
The public health importance of the discovery of H. pylori and its role in stomach diseases was recognized in 2005 by the attribution of the Nobel Prize in Physiology or Medicine to B. Marshall and R. Warren. In the history of Nobel prizes, this is only the third time that the discovery of a bacterium has been acknowledged (Megraud, 2005). For the correct management of peptic ulcer disease and gastric MALT lymphoma, as well as obtaining information on a wide range of diseases associated with H. pylori infection, effective diagnostic methods including susceptibility testing are mandatory. Most of the many different techniques involved in diagnosis of H. pylori infection are performed in microbiology laboratories.
Urinary tract infection (UTI) is a bacterial infection that affects any part of the urinary tract: kidneys, ureters, bladder and urethra (Stamm and Hooton, 1993). Stamm and Hooton, (1993) referred to UTI as a clinical (symptomatic) or subclinical (asymptomatic) disease that may involve just the lower tract or both the lower and upper tracts. Although urine contains a variety of salts and waste products, it usually does not have bacteria in it. But when bacterial gets into the bladder or kidney and multiply in the urine, they cause UTI (Feld et al., 1989; Nicolle et al., 1992). Infection may involve only a single site, such as urethra (urethritis), prostrate (prostatitis), bladder (cystitis), kidney (pyelonephritis) but the whole system is always at risk of invasion by bacteria once any part is infected (Atlas, 1986).
Infections of the urinary tract are one of the most common infections for which antibiotics are prescribed and are among the most frequently occurring infections arising in the hospital setting. Each year UTIs account for more than five to seven million hospital visits, 20 percent of all prescriptions, and require or complicate more than one million hospital admissions in the United States (Schleupner, 1997).
UTI affects all age groups, but women are more exposed than men due to the short urethra, absence of prostatic secretion, pregnancy and easy contamination of the urinary tract with faecal flora (Awaness et al., 2000). Infection particularly in pregnancy and in elderly can be asymptomatic (Al-Dujiaily, 2000) and is associated with an increased risk of intrauterine growth retardation and low birth weight (Harris et al., 1976). Furthermore, untreated asymptomatic bacteriuria can lead to the development of cystitis in approximately 30% of cases, and can lead to the development of pyelonephritis in about 50% of cases (Kass, 1970). Microbiologically, urinary tract infection exists when significant growth of microorganisms is detected in the urinary tract (Tolkoff and Rubin, 1986). The infection is generally considered significant and requires treatment when more than 105 colony forming units per milliliter (105cfu/ml) of urine are present in a properly collected specimen (Kass, 1957; Brooks et al., 2004).

1.2 Justification of Study
Helicobacter pylori (H. pylori) infection is accepted as the primary cause of chronic gastritis (Suerbaum and Michetti, 2002). Moreover, severe atrophic gastritis, accompanying intestinal metaplasia caused by persistent H. pylori infection, is closely related to the development of gastric cancer (Correa, 1992). Although H. pylori was discovered more than 30 years ago by Marshall and Warren (1984), which method should be considered as a gold standard for detection of H. pylori infection, especially for epidemiological studies, remains unclear.
Urinary tract infections (UTIs) are caused by the presence and growth of micro-organisms anywhere in the urinary tract and are perhaps the commonest bacterial infections of mankind (Morgan and Markenzie, 2001; Adeyeba et al., 2002). Urinary tract infection occurs when bacteria is introduced into the urinary system usually through the urethra. When bacteria get into the urinary system they multiply and travel up the urinary tract causing inflammation and irritation along the way (Ayoade et al., 2013). It is one of the most common causes of hospitalization and referral to outpatient, having an estimated figure of 150 million per annum worldwide (Hvidberg et al., 2000; Stamm and Norrby, 2001; Fakhrossadat et al., 2009). Urinary tract infection (UTI) is one of the current infections among teenagers and adults who are sexually active. Screening of asymptomatic subjects for bacteriuria is therefore necessary as bacteriuria has adverse outcomes that can be prevented by antimicrobial therapy (USPSTF, 1996). Apart from that, even the progression of the asymptomatic bacteriuria to the symptomatic UTI in later life can be prevented, which emphasizes the fact that, “prevention is better than cure”.

1.3 Research Questions
1. Do patients with gastritis have H. pylori infection?
2. Do patients with gastritis have urinary tract infection?
3. To what extent does H. pylori infection affect gastritis patients in the study area?
4. To what extent does urinary tract infection affect gastritis patients in the study area?
5. What threats do H. pylori infection and urinary tract infections pose to the health and well-being of these patients?

1.4 Research Hypothesis
• Null Hypothesis (H0): H. pylori infection and urinary tract infections does not affect gastritis patients.
• Alternative (Research) Hypothesis (H1): H. pylori infection and urinary tract infections affects gastritis patients.
1.5 Aim of Study
The aim of this study is to determine and compare the prevalence of H. pylori infection and urinary tract infections among gastritis patients.

1.6 Specific Objectives of the Study
1. To determine the prevalence of H. pylori infection and urinary tract infections among patients with gastritis.
2. To compare the prevalence rates of H. pylori infection and urinary tract infection among patients with gastritis.
4. To ascertain the antimicrobial susceptibility pattern of the isolates.

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