Antibacterial Activity Of Pathogenic Bacteria From Door Handles Of Various Convenience
Microorganisms are found everywhere and constitute the major part of every ecosystem in the environment. They live either freely or as parasite (sleigh and Timbury 1998).
In some cases, they live as transient contaminants in formites or hands when they constitute a major health hazards as source of community and hospital acquired infections (Pettet et al., 1999).
The increasing incidents of epidemic outbreak of certain disease depends on its rate of spread from one community to the other and has then become a major public health concern(Scott et al., Galteli et al., 2006) Although it is acceptable that the infection risk in the general community is less than that associated with patients in the hospital , the yearly increase in food poisoning cases in which households outbreak are a major factor required in the assessment 0of the probable cases and sources (Scott et al., 1982). To place an order for the Complete Project Material, pay N5,000 to Then text the name of the Project topic, email address and your names to 08060565721.
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To place an order for the Complete Project Material, pay N5,000 to
Then text the name of the Project topic, email address and your names to 08060565721.
Besides the day to day interaction of people which constitute in one way of spreading disease, the major source of and spread of community acquired infections are formites (Prescott et al., 1993) Li et al., 2009) formites when in constant contact with humans or natural habitats of pathogenic organism constitute a major source of spread of infectious diseases (Osterholm et al., 1995). Such formites includes : door handles of conveniences , showers, toilet seats, lockers , sinks and tables especially those found in public places like school campuses, hospital and restaurants( Reynolds, 2005). Public toilets have large traffic of users which thongs in with their own microbial flora and other organisms they have picked elsewhere and deposit them on the door handles while going into he convinces and on their way out (Gold hammer et al., 2006)
However the risk of disease transmission through formites is determined by ; the frequency of site contamination and exposure; level of pathogen excreted by the host; likelihood of transfer of the infectious agent to a susceptible individual; virulence of organism; immune-competence of the persons in contact; the practice of control measure such as disinfectant use and personal hygiene. (Reynolds, 2005)
1.1 Statement of Problem
Unfortunately, majority of public toilets found in campuses lack water system and where there are such systems water is never available. Consequently, users can hardly wash their hands after usage carrying their contaminants from such conveniences (Guannini et al., 2009) and such could result to outbreak of cholera and staphlylococcus aurues (A.MRSA) in prevalence areas.
1.2 Aims of the Study
To investigate the antibacterial activity of various hand sanitizer on bacteria isolated from door handles of conveniece
1.3 Objective of the study
The objectives of this study are as follows:
a. To isolate microorganism from door handles of conveniences and to identify the isolates.
b. To determine the antibacterial activity of hand sanitizers on the isolates.
c. To advise the students using the conveniences on the dangers associated with improper usage of conveniences
2.1 Staphylococcus aureus
Staphylococcus aureus is a Gram-positive coccal bacterium that is a member of the Firmicutes, and is frequently found in the human respiratory tract and on the skin. It is positive for catalase and nitrate reduction. Although S. aureus is not always pathogenic, it is a common cause of skin infections (e.g. boils), respiratory disease (e.g. sinusitis), and food poisoning. Disease-associated strains often promote infections by producing potent protein toxins, and expressing cell-surface proteins that bind and inactivate antibodies. The emergence of antibiotic-resistant forms of pathogenic S. aureus (e.g. MRSA) is a worldwide problem in clinical medicine.
Staphylococcus was first identified in 1880 in Aberdeen, United Kingdom, by the surgeon Sir Alexander Ogston in pus from a surgical abscess in a knee joint (Ogston, 1998). This name was later appended to Staphylococcus aureus by Rosenbach who was credited by the official system of nomenclature at the time. It is estimated that 20% of the human population are long-term carriers of S. aureus which can be found as part of the normal skin flora and in anterior nares of the nasal passages. S. aureus is the most common species of staphylococcus to cause Staph infections and is a successful pathogen due to a combination of nasal carriage and bacterial immuno-evasive strategies. S. aureus can cause a range of illnesses, from minor skin infections, such as pimples, impetigo, boils (furuncles), cellulitis folliculitis, carbuncles, scalded skin syndrome, and abscesses, to life-threatening diseases such as pneumonia, meningitis, osteomyelitis, endocarditis, toxic shock syndrome (TSS), bacteremia, and sepsis. Its incidence ranges from skin, soft tissue, respiratory, bone, joint, endovascular to wound infections. It is still one of the five most common causes of nosocomial infections and is often the cause of postsurgical wound infections. Each year, some 500,000 patients in United States’ hospitals contract a staphylococcal infection (Ryan, Ray, 2004).
2.2 Role of staphylococcal in diseases
S. aureus is responsible for many infections but it may also occur as a commensal. The presence of S. aureus does not always indicate infection. S. aureus can survive from hours to weeks, or even months, on dry environmental surfaces, depending on strain (Matthews et al., 1997).
S. aureus can infect tissues when the skin or mucosal barriers have been breached. This can lead to many different types of infections including furuncles and carbuncles (a collection of furuncles).
S. aureus infections can spread through contact with pus from an infected wound, skin-to-skin contact with an infected person by producing hyaluronidase that destroys tissues, and contact with objects such as towels, sheets, clothing, or athletic equipment used by an infected person.
2.1.1 Atopic dermatitis
S. aureus is extremely prevalent in persons with atopic dermatitis. It is mostly found in fertile, active places, including the armpits, hair, and scalp. Large pimples that appear in those areas may exacerbate the infection if lacerated. This can lead to staphylococcal scalded skin syndrome (SSSS). A severe form of this, Ritter’s disease, can be observed in neonates (Birnie, Bath-Hextall, Ravenscroft, Williams, 2008).
The presence of S. aureus in persons with atopic dermatitis is not an indication to treat with oral antibiotics, as evidence has not shown this to give benefit to the patient. The relationship between S.aureus and atopic dermatitis is unclear. Evidence shows that attempting to control S. aureus with oral antibiotics is not efficacious (Cenci-Goga et al., 2003).
2.2 Virulence factors
Staphylococcus aureus produces various enzymes such as coagulase (bound and free coagulases) which clots plasma and coats the bacterial cell to probably prevent phagocytosis. Hyaluronidase (also known as spreading factor) breaks down hyaluronic acid and helps in spreading of Staphylococcus aureus. S.aureus also produces DNAse (deoxyribonuclease) which breaks down the DNA, lipase to digest lipids, staphylokinase to dissolve fibrin and aid in spread, and beta-lactamase for drug resistance (Matthews, Roberson, Gillespie, Luther, Oliver,1997)
Depending on the strain, S. aureus is capable of secreting several exotoxins, which can be categorized into three groups. Many of these toxins are associated with specific diseases (Ryan, Ray, 2004)
2.2.3 Exfoliative toxins
EF toxins are implicated in the disease staphylococcal scalded-skin syndrome (SSSS), which occurs most commonly in infants and young children. It also may occur as epidemics in hospital nurseries. The protease activity of the exfoliative toxins causes peeling of the skin observed with SSSS.
2.2.4 Other toxins
Staphylococcal toxins that act on cell membranes include alpha toxin, beta toxin, delta toxin, and several bicomponent toxins. The bicomponent toxin Panton-Valentine leukocidin (PVL) is associated with severe necrotizing pneumonia in children.The genes encoding the components of PVL are encoded on a bacteriophage found in community-associated methicillin-resistant S. aureus (MRSA) strains.
2.3 Escherichia coli
Escherichia coli (commonly abbreviated E. coli) is a Gram-negative, facultatively anaerobic, rod-shaped bacterium of the genus Escherichia that is commonly found in the lower intestine of warm-blooded organisms (endotherms).Most E. coli strains are harmless, but some serotypes can cause serious food poisoning in their hosts, and are occasionally responsible for product recalls due to food contamination(Bentley and Meganathan 1982) The harmless strains are part of the normal flora of the gut, and can benefit their hosts by producing vitamin K2, and preventing colonization of the intestine with pathogenic bacteria.( Hudault et al ., 2001).
E. coli and other facultative anaerobes constitute about 0.1% of gut flora, (Reid et al ., 2001) and fecal–oral transmission is the major route through which pathogenic strains of the bacterium cause disease. Cells are able to survive outside the body for a limited amount of time, which makes them ideal indicator organisms to test environmental samples for fecal contamination (Reid et al., 2001). A growing body of research, though, has examined environmentally persistent E. coli which can survive for extended periods outside of a host.
The bacterium can be grown easily and inexpensively in a laboratory setting, and has been intensively investigated for over 60 years. E. coli is the most widely studied prokaryotic model organism, and an important species in the fields of biotechnology and microbiology, where it has served as the host organism for the majority of work with recombinant DNA. Under favourable conditions, it takes only 20 minutes to reproduce.( Reid et al., 2001).
Biology and biochemistry
E. coli is Gram-negative (bacteria which do not retain crystal violet dye), facultative anaerobic (that makes ATP by aerobic respiration if oxygen is present, but is capable of switching to fermentation or anaerobic respiration if oxygen is absent) and nonsporulating ( Lawrence and Ochman 1998). Cells are typically rod-shaped, and are about 2.0 micrometers (μm) long and 0.25–1.0 μm in diameter, with a cell volume of 0.6–0.7 μm3. It can live on a wide variety of substrates. E. coli uses mixed-acid fermentation in anaerobic conditions, producing lactate, succinate, ethanol, acetate, and carbon dioxide. Since many pathways in mixed-acid fermentation produce hydrogen gas, these pathways require the levels of hydrogen to be low, as is the case when E. coli lives together with hydrogen-consuming organisms, such as methanogens or sulphate-reducing bacteria.
Optimal growth of E. coli occurs at 37 °C (98.6 °F), but some laboratory strains can multiply at temperatures of up to 49 °C. Growth can be driven by aerobic or anaerobic respiration, using a large variety of redox pairs, including the oxidation of pyruvic acid, formic acid, hydrogen, and amino acids, and the reduction of substrates such as oxygen, nitrate, fumarate, dimethyl sulfoxide, and trimethylamine N-oxide.Strains that possess flagella are motile. The flagella have a peritrichous arrangement (Han and Lee, 2006)
E. coli and related bacteria possess the ability to transfer DNA via bacterial conjugation, transduction or transformation, which allows genetic material to spread horizontally through an existing population. This process led to the spread of the gene encoding shiga toxin from Shigella to E. coli O157:H7, carried by a bacteriophage.
Escherichia coli encompass an enormous population of bacteria that exhibit a very high degree of both genetic and phenotypic diversity. Genome sequencing of a large number of isolates of E. coli and related bacteria shows that a taxonomic reclassification would be desirable. However, this has not been done, largely due to its medical importance (Reid et al., 2001) and E. coli remains one of the most diverse bacterial species: only 20% of the genome is common to all strains. In fact, from the evolutionary point of view, the members of genus Shigella (S. dysenteriae, S. flexneri, S. boydii, and S. sonnei) should be classified as E. coli strains, a phenomenon termed taxa in disguise.( Reid et al., 2001). Similarly, other strains of E. coli (e.g. the K-12 strain commonly used in recombinant DNA work) are sufficiently different that they would merit reclassification.
A strain is a subgroup within the species that has unique characteristics that distinguish it from other strains. These differences are often detectable only at the molecular level; however, they may result in changes to the physiology or lifecycle of the bacterium. For example, a strain may gain pathogenic capacity, the ability to use a unique carbon source, the ability to take upon a particular ecological niche, or the ability to resist antimicrobial agents. Different strains of E. coli are often host-specific, making it possible to determine the source of fecal contamination in environmental samples.( Hudault et al .,2001) For example, knowing which strains are present in a water sample allows researchers to make assumptions about whether the contamination originated from a human, another mammal, or a bird.
A common subdivision system of E. coli, but not based on evolutionary relatedness, is by serotype, which is based on major surface antigens (O antigen: part of lipopolysaccharide layer; H: flagellin; K antigen: capsule), e.g. O157:H7).It is, however, common to cite only the serogroup, i.e. the O-antigen. At present, about 190 serogroups are known. The common laboratory strain has a mutation that prevents the formation of an O-antigen and is thus not typeable.
Genome plasticity and evolution
Like all lifeforms, new strains of E. coli evolve through the natural biological processes of mutation, gene duplication, and horizontal gene transfer in particular 18% of the genome of the laboratory strain MG1655 was horizontally acquired since the divergence from Salmonella. E. coli K-12 and E. coli B strains are the most frequently used varieties for laboratory purposes. Some strains develop traits that can be harmful to a host animal. These virulent strains typically cause a bout of diarrhea that is unpleasant in healthy adults and is often lethal to children in the developing world. More virulent strains, such as O157:H7, cause serious illness or death in the elderly, the very young, or the immune-compromised. (Hudault et al., 2001).
The genera Escherichia and Salmonella diverged around 102 million years ago (credibility interval: 57–176 mya), which coincides with the divergence of their hosts: the former being found in mammals and the latter in birds and reptiles.
This was followed by a split of the escherichian ancestor into five species (E. albertii, E. coli, E. fergusonii, E. hermannii, and E. vulneris.) The last E. coli ancestor split between 20 and 30 million years ago.
The long-term evolution experiments using E. coli, begun by Richard Lenski in 1988, have allowed direct observation of major evolutionary shifts in the laboratory. In this experiment, one population of E. coli unexpectedly evolved the ability to aerobically metabolize citrate, which is extremely rare in E. coli. As the inability to grow aerobically is normally used as a diagnostic criterion with which to differentiate E. coli from other, closely related bacteria, such as Salmonella, this innovation may mark a speciation event observed in the laboratory.
E. coli is the type species of the genus (Escherichia) and in turn Escherichia is the type genus of the family Enterobacteriaceae, where the family name does not stem from the genus Enterobacter + “i” (sic.) + “aceae”, but from “enterobacterium” + “aceae” (enterobacterium being not a genus, but an alternative trivial name to enteric bacterium).
The original strain described by Escherichia is believed to be lost, consequently a new type strain (neotype) was chosen as a representative: the neotype strain is ATCC 11775, also known as NCTC 9001, which is pathogenic to chickens and has an O1:K1:H7 serotype. However, in most studies, either O157:H7, K-12 MG1655, or K-12 W3110 are used as a representative E. coli.
A large number of strains belonging to this species have been isolated and characterised. In addition to serotype (vide supra), they can be classified according to their phylogeny, i.e. the inferred evolutionary history, as shown below where the species is divided into six groups.
The link between phylogenetic distance (“relatedness”) and pathology is small, e.g. the O157:H7 serotype strains, which form a clade (“an exclusive group”)—group E below—are all enterohaemorragic strains (EHEC), but not all EHEC strains are closely related. In fact, four different species of Shigella are nested among E. coli strains (vide supra), while E. albertii and E. fergusonii are outside of this group. All commonly used research strains of E. coli belong to group A and are derived mainly from Clifton’s K-12 strain (λ⁺ F⁺; O16) and to a lesser degree from d’Herelle’s Bacillus coli strain (B strain).
The first complete DNA sequence of an E. coli genome (laboratory strain K-12 derivative MG1655) was published in 1997. It was found to be a circular DNA molecule 4.6 million base pairs in length, containing 4288 annotated protein-coding genes (organized into 2584 operons), seven ribosomal RNA (rRNA) operons, and 86 transfer RNA (tRNA) genes. Despite having been the subject of intensive genetic analysis for about 40 years, a large number of these genes were previously unknown. The coding density was found to be very high, with a mean distance between genes of only 118 base pairs. The genome was observed to contain a significant number of transposable genetic elements, repeat elements, cryptic prophages, and bacteriophage remnants.
Today, over 60 complete genomic sequences of Escherichia and Shigella species are available. Comparison of these sequences shows a remarkable amount of diversity; only about 20% of each genome represents sequences present in every one of the isolates, while around 80% of each genome can vary among isolates. Each individual genome contains between 4,000 and 5,500 genes, but the total number of different genes among all of the sequenced E. coli strains (the pangenome) exceeds 16,000. This very large variety of component genes has been interpreted to mean that two-thirds of the E. coli pangenome originated in other species and arrived through the process of horizontal gene transfer.
Role in disease
Pathogenic Escherichia coli
Most E. coli strains do not cause disease, but virulent strains can cause gastroenteritis, urinary tract infections, and neonatal meningitis. In rarer cases, virulent strains are also responsible for hemolytic-uremic syndrome, peritonitis, mastitis, septicemia, and Gram-negative pneumonia.
Uropathogenic E. coli (UPEC) is one of the main causes of urinary tract infections. It is part of the normal flora in the gut and can be introduced in many ways. In particular for females, the direction of wiping after defecation (wiping back to front) can lead to fecal contamination of the urogenital orifices. Anal intercourse can also introduce this bacterium into the male urethra, and in switching from anal to vaginal intercourse, the male can also introduce UPEC to the female urogenital system. For more information, see the databases at the end of the article or UPEC
In May 2011, one E. coli strain, O104:H4, has been the subject of a bacterial outbreak that began in Germany. Certain strains of E. coli are a major cause of foodborne illness. The outbreak started when several people in Germany were infected with enterohemorrhagic E. coli (EHEC) bacteria, leading to hemolytic-uremic syndrome (HUS), a medical emergency that requires urgent treatment. The outbreak did not only concern Germany, but also 11 other countries, including regions in North America. On 30 June 2011, the German Bundesinstitut für Risikobewertung (BfR) (Federal Institute for Risk Assessment, a federal institute within the German Federal Ministry of Food, Agriculture and Consumer Protection) announced that seeds of fenugreek from Egypt were likely the cause of the EHEC outbreak.
In 1885, the German-Austrian pediatrician Theodor Escherichia discovered this organism in the feces of healthy individuals and called it Bacterium coli commune because it is found in the colon and early classifications of prokaryotes placed these in a handful of genera based on their shape and motility (at that time Ernst Haeckel’s classification of Bacteria in the kingdom Monera was in place(Hudault et al .,2001). Bacterium coli was the type species of the now invalid genus Bacterium when it was revealed that the former type species (“Bacterium triloculare”) was missing. Following a revision of Bacterium, it was reclassified as Bacillus coli by (Migula et al., 1995) and later reclassified in the newly created genus Escherichia, named after its original discoverer.
Pseudomonas is a genus of Gram-negative, aerobic gammaproteobacteria, belonging to the family Pseudomonadaceae containing 191 validly described species. The members of the genus demonstrate a great deal of metabolic diversity, and consequently are able to colonize a wide range of niches. Their ease of culture in vitro and availability of an increasing number of Pseudomonas strain genome sequences has made the genus an excellent focus for scientific research; the best studied species include P. aeruginosa in its role as an opportunistic human pathogen, the plant pathogen P. syringae, the soil bacterium P. putida, and the plant growth-promoting P. fluorescens.
Because of their widespread occurrence in water and plant seeds such as dicots, the pseudomonads were observed early in the history of microbiology. The generic name Pseudomonas created for these organisms was defined in rather vague terms by Walter Migula in 1894 and 1900 as a genus of Gram-negative, rod-shaped and polar-flagellated bacteria with some sporulating species, the latter statement was later proved incorrect and was due to refractive granules of reserve materials. Despite the vague description, the type species, Pseudomonas pyocyanea (basonym of Pseudomonas aeruginosa), proved the best descriptor.
Like most bacterial genera, the pseudomonad last common ancestor lived hundreds of millions of years ago. They were initially classified at the end of the 19th century when first identified by Walter Migula. The etymology of the name was not specified at the time and first appeared in the seventh edition of Bergey’s Manual of Systematic Bacteriology (the main authority in bacterial nomenclature) however, Migula possibly intended it as false Monas, a nanoflagellated protist (subsequently, the term “monad” was used in the early history of microbiology to denote unicellular organisms). Soon, other species matching Migula’s somewhat vague original description were isolated from many natural niches and, at the time, many were assigned to the genus. However, many strains have since been reclassified, based on more recent methodology and use of approaches involving studies of conservative macromolecules.
Recently, 16S rRNA sequence analysis has redefined the taxonomy of many bacterial species. As a result, the genus Pseudomonas includes strains formerly classified in the genera Chryseomonas and Flavimonas. Other strains previously classified in the genus Pseudomonas are now classified in the genera Burkholderia and Ralstonia.
In 2000, the complete genome sequence of a Pseudomonas species was determined; more recently, the sequence of other strains has been determined, including P. aeruginosa strains PAO1 (2000), P. putida KT2440 (2002), P. protegens Pf-5 (2005), P. syringae pathovar tomato DC3000 (2003), P. syringae pathovar syringae B728a (2005), P. syringae pathovar phaseolica 1448A (2005), P. fluorescens Pf0-1, and P. entomophila L48.
Pseudomonas may be the most common nucleator of ice crystals in clouds, thereby being of utmost importance to the formation of snow and rain around the world.
Members of the genus display these defining characteristics:
· One or more polar flagella, providing motility
· Positive catalase test
· Positive oxidase test
Other characteristics that tend to be associated with Pseudomonas species (with some exceptions) include secretion of pyoverdine, a fluorescent yellow-green siderophoreunder iron-limiting conditions. Certain Pseudomonas species may also produce additional types of siderophore, such as pyocyanin by Pseudomonas aeruginosa and thioquinolobactin by Pseudomonas fluorescens,
Pseudomonas species also typically give a positive result to the oxidase test, the absence of gas formation from glucose, glucose is oxidised in oxidation/fermentation test using Hugh and Leifson O/F test, beta hemolytic (on blood agar), indole negative, methyl red negative, Voges–Proskauer test negative, and citrate positive(Cornelis 2008).
All species and strains of Pseudomonas have historically been classified as strict aerobes. Exceptions to this classification have recently been discovered in Pseudomonas biofilm (Madigan and Martinko, 2005). . A significant number of cells can produce exopolysaccharides associated with biofilm formation. Secretion of exopolysaccharides such as alginate makes it difficult for pseudomonads to be phagocytosed by mammalian white blood cells. Exopolysaccharide production also contributes to surface-colonising biofilms that are difficult to remove from food preparation surfaces. Growth of pseudomonads on spoiling foods can generate a “fruity” odor.
Pseudomonas species have the ability to metabolize a variety of nutrients. Combined with the ability to form biofilms, they are, thus, able to survive in a variety of unexpected places. For example, they have been found in areas where pharmaceuticals are prepared. A simple carbon source, such as soap residue or cap liner-adhesives is a suitable place for them to thrive. Other unlikely places where they have been found include antiseptics, such as quaternary ammonium compounds, and bottled mineral water.
Being Gram-negative bacteria, most Pseudomonas spp. are naturally resistant to penicillin and the majority of related beta-lactam antibiotics, but a number are sensitive to piperacillin, imipenem, ticarcillin, or ciprofloxacin. Aminoglycosides such as tobramycin, gentamicin, and amikacin are other choices for therapy.
This ability to thrive in harsh conditions is a result of their hardy cell walls that contain porins. Their resistance to most antibiotics is attributed to efflux pumps, which pump out some antibiotics before they are able to act.
Pseudomonas aeruginosa is increasingly recognized as an emerging opportunistic pathogen of clinical relevance. One of its most worrying characteristics is its low antibiotic susceptibility. This low susceptibility is attributable to a concerted action of multidrug efflux pumps with chromosomally encoded antibiotic resistance genes (e.g., mexAB-oprM, mexXY, etc.,) (Madigan and Martinko, 2005) and the low permeability of the bacterial cellular envelopes. Besides intrinsic resistance, P. aeruginosa easily develops acquired resistance either by mutation in chromosomally encoded genes or by the horizontal gene transfer of antibiotic resistance determinants. Development of multidrug resistance by P. aeruginosa isolates requires several different genetic events that include acquisition of different mutations and/or horizontal transfer of antibiotic resistance genes. Hypermutation favours the selection of mutation-driven antibiotic resistance in P. aeruginosa strains producing chronic infections, whereas the clustering of several different antibiotic resistance genes in integrons favours the concerted acquisition of antibiotic resistance determinants. Some recent studies have shown phenotypic resistance associated to biofilm formation or to the emergence of small-colony-variants may be important in the response of P. aeruginosa populations to antibiotic treatment.
The studies on the taxonomy of this complicated genus groped their way in the dark while following the classical procedures developed for the description and identification of the organisms involved in sanitary bacteriology during the first decades of the 20th century. This situation sharply changed with the proposal to introduce as the central criterion the similarities in the composition and sequences of macromolecular components of the ribosomal RNA. The new methodology clearly showed the genus Pseudomonas, as classically defined, consists of a conglomerate of genera that could clearly be separated into five so-called rRNA homology groups. Moreover, the taxonomic studies suggested an approach that might prove useful in taxonomic studies of all other prokaryotic groups. A few decades after the proposal of the new genus Pseudomonas by Migula in 1894, the accumulation of species names assigned to the genus reached alarming proportions. The number of species in the current list has contracted more than 90%. In fact, this approximated reduction may be even more dramatic if one considers the present list contains many new names; i.e., relatively few names of the original list survived in the process. The new methodology and the inclusion of approaches based on the studies of conservative macromolecules other than rRNA components constitute an effective prescription that helped to reduce Pseudomonas nomenclatural hypertrophy to a manageable size.
Infectious species include P. aeruginosa, P. oryzihabitans, and P. plecoglossicida. P. aeruginosa flourishes in hospital environments, and is a particular problem in this environment, since it is the second-most common infection in hospitalized patients (nosocomial infections). This pathogenesis may in part be due to the proteins secreted by P. aeruginosa. The bacterium possesses a wide range of secretion systems, which export numerous proteins relevant to the pathogenesis of clinical strains. (Yabuuchi et al., 2005)
P. syringae is a prolific plant pathogen. It exists as over 50 different pathovars, many of which demonstrate a high degree of host-plant specificity. Numerous other Pseudomonas species can act as plant pathogens, notably all of the other members of the P. syringae subgroup, but P. syringae is the most widespread and best-studied.
Although not strictly a plant pathogen, P. tolaasii can be a major agricultural problem, as it can cause bacterial blotch of cultivated mushrooms.Similarly, P. agarici can cause drippy gill in cultivated mushrooms
Use as biocontrol agents
Since the mid-1980s, certain members of the Pseudomonas genus have been applied to cereal seeds or applied directly to soils as a way of preventing the growth or establishment of crop pathogens. This practice is generically referred to as biocontrol. The biocontrol properties of P. fluorescens and P. protegens strains (CHA0 or Pf-5 for example) are currently best-understood, although it is not clear exactly how the plant growth-promoting properties of P. fluorescens are achieved. Theories include: the bacteria might induce systemic resistance in the host plant, so it can better resist attack by a true pathogen; the bacteria might outcompete other (pathogenic) soil microbes, e.g. by siderophores giving a competitive advantage at scavenging for iron; the bacteria might produce compounds antagonistic to other soil microbes, such as phenazine-type antibiotics or hydrogen cyanide. Experimental evidence supports all of these theories.
Other notable Pseudomonas species with biocontrol properties include P. chlororaphis, which produces a phenazine-type antibiotic active agent against certain fungal plant pathogens,and the closely related species P. aurantiaca, which produces di-2,4-diacetylfluoroglucylmethane, a compound antibiotically active against Gram-positive organisms.
Use as bioremediation agents
Some members of the genus are able to metabolise chemical pollutants in the environment, and as a result, can be used for bioremediation. Notable species demonstrated as suitable for use as bioremediation agents include:
· P. alcaligenes, which can degrade polycyclic aromatic hydrocarbons.
· P. mendocina, which is able to degrade toluene.
· P. pseudoalcaligenes, which is able to use cyanide as a nitrogen source.
· P. resinovorans, which can degrade carbazole.
· P. veronii, which has been shown to degrade a variety of simple aromatic organic compounds.
· P. putida, which has the ability to degrade organic solvents such as toluene. At least one strain of this bacterium is able to convert morphine in aqueous solution into the stronger and somewhat expensive to manufacture drug hydromorphone (Dilaudid) (Madigan and Martinko 2005).
Strain KC of P. stutzeri, which is able to degrade carbon tetrachloride. Food spoilage agents
As a result of their metabolic diversity, ability to grow at low temperatures, and ubiquitous nature, many Pseudomonas species can cause food spoilage. Notable examples include dairy spoilage by P. fragi, mustiness in eggs caused by P. taetrolens and P. mudicolens,and P. lundensis, which causes spoilage of milk, cheese, meat, and fish. (Yabuuchi et al., 2005)
2.5 Klebsiella species
Klebsiella is a genus of non-motile, Gram-negative, oxidase-negative, rod-shaped bacteria with a prominent polysaccharide-based capsule (Ryan and Ray, 2004) It is named after the German microbiologist Edwin Klebs (1834–1913).
Klebsiella species are found everywhere in nature. This is thought to be due to distinct sublineages developing specific niche adaptations, with associated biochemical adaptations which make them better suited to a particular environment. They can be found in water, soil, plants, insects, animals and humans
2.1 Features of Klebsiella species
Klebsiella bacteria tend to be rounder and thicker than other members of the Enterobacteriaceae family. They typically occur as straight rods with rounded or slightly pointed ends. They can be found singly, in pairs or in short chains. Diplobacillary forms are commonly found in vivo (Brisse et al., 2004).
They have no specific growth requirements and grow well on standard laboratory media, but grow best between 35 and 37ºC and at pH 7.2. The species are facultative anaerobes, and most strains can survive with citrate and glucose as their sole carbon sources and ammonia as their sole nitrogen source.
Members of the genus produce a prominent capsule, or slime layer, which can be used for serologic identification, but molecular serotyping may replace this method (Podschun and Ullmann, 1998).
2.4.2 Klebsiella in humans
Klebsiella species are routinely found in the human nose, mouth, and gastrointestinal tract as normal flora; however, they can also behave as opportunistic human pathogens. Klebsiella species are known to also infect a variety of other animals, both as normal flora and opportunistic pathogens.
Klebsiella organisms can lead to a wide range of disease states, notably pneumonia, urinary tract infections, septicemia, meningitis, diarrhea, and soft tissue infections ((Podschun and Ullmann,1998). Klebsiella species have also been implicated in the pathogenesis of ankylosing spondylitis and other spondyloarthropathies. The majority of human Klebsiella infections are caused by K. pneumoniae, followed by K. oxytoca. Infections are more common in the very young, very old, and those with other underlying diseases, such as cancer, and most infections involve contamination of an invasive medical device.
During the last 40 years, many trials for constructing effective K. pneumoniae vaccines have been tried. Currently, no Klebsiella vaccine has been licensed for use in the US. K. pneumoniae is the most common cause of nosocomial respiratory tract and premature intensive care infections, and the second-most frequent cause of Gram-negative bacteraemia and urinary tract infections. Drug-resistant isolates remain an important hospital-acquired bacterial pathogen, add significantly to hospital stays, and are especially problematic in high-impact medical areas such as intensive care units. This antimicrobial resistance is thought to be attributable mainly to multidrug efflux pumps. The ability of K. pneumoniae to colonize the hospital environment, including carpeting, sinks, flowers, and various surfaces, as well as the skin of patients and hospital staff, has been identified as a major factor in the spread of hospital-acquired infections.
2.5 Transmission route of pathogenic bacteria
A classic characteristic of human parasitic and bacterial agents is the evolution of routes for transmission to susceptible hosts. The environment plays a critical role in transmission to humans, with many environmental materials serving as vehicles (Anderson & May, 1991; Struthers Westran, 2003). Microbial contaminants may be transmitted directly, through hand-to-hand contact, or indirectly, via food or other inanimate objects. These routes of transmission are of great importance in the health of many populations in developing countries, where the frequency of infection is a general indication of local hygiene and environmental sanitation levels (Cooper, 1991).
With a number of infectious intestinal diseases, a low dose of the infectious agent is capable of causing illness; therefore. failure of food service workers to adequately sanitize hands or use food-handling tools (tongs, spoons. utensils or bakety/serving papers) between the handling of money and the serving of food could put food service patrons at risk (Michaels, 2002).
Oddly, publications regarding the degree to which paper money is contaminated with bacteria are few and far between, as the authors found when they conducted a Medline search in December 2005 (Abrams and Waterman, 1972; El-Dars and Hassan, 2005). Furthermore, the search found no documented study of the parasitological status of currency notes (as of December 2005). Scientific information on the contamination of money by microbial agents is also lacking in most developing countries in sub-Saharan Africa, including Nigeria This dearth of information may have contributed to the absence of public health policies or legislation on currency usage, handling, and circulation in many parts of Africa Although the studies done in the United States and Australia have had no major impact on policies or legislation on currency handling and circulation in those countries, they have fostered a higher level of public awareness about the potential for currency contamination by microorganisms (Dow Jones News, 1998).
Shigella is a genus of Gram-negative, facultative anaerobic, nonspore-forming, nonmotile, rod-shaped bacteria closely related to Salmonella. The genus is named after Kiyoshi Shiga, who first discovered it in 1897 (Yabuuchi 2002).
The causative agent of human shigellosis, Shigella causes disease in primates, but not in other mammals.[Ryan et al., 2004) It is only naturally found in humans and apes. During infection, it typically causes dysentery. Shigella is one of the leading bacterial causes of diarrhea worldwide. Insufficient data exist, but conservative estimates suggest Shigella causes about 90 million cases of severe dysentery, with at least 100,000 of these resulting in death, each year, mostly among children in the developing world.
· Shigella species are classified by four serogroups:
· serogroup A: S. dysenteriae (15 serotypes)
· Serogroup B: S. flexneri (six serotypes)
· Serogroup C: S. boydii (19 serotypes)
· Serogroup D: S. sonnei (one serotype) (Yabuuchi et al., 2005)
Groups A–C are physiologically similar; S. sonnei (group D) can be differentiated on the basis of biochemical metabolism assays. Three Shigella groups are the major disease-causing species: S. flexneri is the most frequently isolated species worldwide, and accounts for 60% of cases in the developing world; S. sonnei causes 77% of cases in the developed world, compared to only 15% of cases in the developing world; and S. dysenteriae is usually the cause of epidemics of dysentery, particularly in confined populations such as refugee camps.
Each of the Shigella genomes includes a virulence plasmid that encodes conserved primary virulence determinants. The Shigella chromosomes share most of their genes with those of E. coli K12 strain MG1655. Phylogenetic studies indicate Shigella is more appropriately treated as subgenus of Escherichia, and that certain strains generally considered E. coli – such as E. coli O157:H7 – are better placed in Shigella
Shigella infection is typically by ingestion (fecal–oral contamination); depending on age and condition of the host, fewer than 100 bacterial cells can be enough to cause an infection. Shigella causes dysentery that result in the destruction of the epithelial cells of the intestinal mucosa in the cecum and rectum. Some strains produce the enterotoxin shiga toxin, which is similar to the verotoxin of E. coli O157:H7 and other verotoxin-producing E. coli. Both shiga toxin and verotoxin are associated with causing hemolytic uremic syndrome. As noted above, these supposed E. coli strains are at least in part actually more closely related to Shigella than to the “typical” E. coli.
Shigella species invade the host through the M-cells interspersed in the gut epithelia of the small intestine, as they do not interact with the apical surface of epithelial cells, preferring the basolateral side. Shigella uses a type-III secretion system, which acts as a biological syringe to translocate toxic ( Potter, 2006) effector proteins to the target human cell. The effector proteins can alter the metabolism of the target cell, for instance leading to the lysis of vacuolar membranes or reorganization of actin polymerization to facilitate intracellular motility of Shigella bacteria inside the host cell . For instance, the IcsA effector protein triggers actin reorganization by N-WASP recruitment of Arp2/3 complexes, helping cell-to-cell spread.
After invasion, Shigella cells multiply intracellularly and spread to neighboring epithelial cells, resulting in tissue destruction and characteristic pathology of shigellosis.
The most common symptoms are diarrhea, fever, nausea, vomiting, stomach cramps, and flatulence. It is also commonly known to cause large and painful bowel movements. The stool may contain blood, mucus, or pus. Hence, Shigella cells may cause dysentery. In rare cases, young children may have seizures. Symptoms can take as long as a week to appear, but most often begin two to four days after ingestion. Symptoms usually last for several days, but can last for weeks. Shigella is implicated as one of the pathogenic causes of reactive arthritis worldwide. (Mims et al.,1993)
The diagnosis of shigellosis is made by isolating the organism from diarrheal fecal sample cultures. Shigella species are negative for motility and are generally not lactose fermenters, but S. sonnei can ferment lactose. They typically do not produce gas from carbohydrates (with the exception of certain strains of S. flexneri) and tend to be overall biochemically inert. Shigella should also be urea hydrolysis negative. When inoculated to a triple sugar iron (TSI) slant, they react as follows: K/A, gas -, and H2S -. Indole reactions are mixed, positive and negative, with the exception of S. sonnei, which is always indole negative. Growth on Hektoen enteric agar will produce bluish-green colonies for Shigella and bluish-green colonies with black centers for Salmonella (Yang et al., 2005)
Prevention and treatment
Hand washing before handling food and thoroughly cooking all food before eating decreases the risk of getting shigellosis.
Severe dysentery can be treated with ampicillin, TMP-SMX, or fluoroquinolones, such as ciprofloxacin, and of course rehydration. Medical treatment should only be used in severe cases or for certain populations with mild symptoms (elderly, immunocompromised, food service industry workers, child care workers). Antibiotics are usually avoided in mild cases because some Shigella species are resistant to antibiotics, and their use may make the bacteria even more resistant. Antidiarrheal agents may worsen the sickness, and should be avoided. For Shigella-associated diarrhea, antibiotics shorten the length of infection. (Mims et al., 1993)
Currently, no licenced vaccine targeting Shigella exists. Shigella has been a longstanding World Health Organization target for vaccine development, and sharp declines in age-specific diarrhea/dysentery attack rates for this pathogen indicate natural immunity does develop following exposure; thus, vaccination to prevent the disease should be feasible. Several vaccine candidates for Shigella are in various stages of development.
Salmonella is a genus of rod-shaped, Gram-negative bacteria. There are only two species of Salmonella, Salmonella bongori and Salmonella enterica, of which there are around six subspecies and innumerable serovars. The genus belongs to the same family as Escherichia, which includes the species E.coli.
Salmonellae are found worldwide in both cold-blooded and warm-blooded animals, and in the environment.( Ryan and Ray 2004) They cause illnesses such as typhoid fever, paratyphoid fever, and food poisoning.
Salmonella are non-spore-forming, predominantly motile enterobacteria with diameters around 0.7 to 1.5 µm, lengths from 2 to 5 µm, and peritrichous flagella (flagella that are all around the cell body). They are chemoorganotrophs, obtaining their energy from oxidation and reduction reactions using organic sources, and are facultative anaerobes (Fabrega and Vila 2013)
The story of the term Salmonella started in 1885 with the discovery of the bacterium Salmonella enterica (var. Choleraesuis) by medical research scientist Theobald Smith. At the time Theobald was working as a research laboratory assistant in the Veterinary Division of the United States Department of Agriculture. The department was under the administration of Daniel Elmer Salmon, a veterinary pathologist, and that is for whom the Salmonella was named.
During the search for the cause of hog cholera it was proposed that the causal agent be named Salmonella. While it happened eventually that Salmonella did not cause that cholera (its enteric pathogen was actually a virus),it turned out that all species of the bacterial genus Salmonella cause infectious diseases. In 1900 J. Lignières re-adopted the name for the many subspecies of Salmonella, after Smith’s first type-strain Salmonella cholera.( Winfield et al.,2003)
Detection, culture and growth condition
Most subspecies of Salmonella produce hydrogen sulfide, which can readily be detected by growing them on media containing ferrous sulfate, such as is used in the triple sugar iron test (TSI). Most isolates exist in two phases: a motile phase I and a nonmotile phase II. Cultures that are nonmotile upon primary culture may be switched to the motile phase using a Cragie tube.
Salmonella can also be detected and subtyped using PCR from extracted salmonella DNA, various methods are available to extract salmonella DNA from target samples.
Mathematical models of salmonella growth kinetics have been developed for chicken, pork, tomatoes, and melons. Salmonella reproduce asexually with a cell division rate of 20 to 40 minutes under optimal conditions.
Salmonella lead predominantly host-associated lifestyles, however the bacteria were found to be able to persist in a bathroom setting for weeks following contamination, and are frequently isolated from water sources, which act as bacterial reservoirs and may help to facilitate transmission between hosts. The bacteria are not destroyed by freezing, but UV light and heat accelerate their demise—they perish after being heated to 55 °C (131 °F) for 90 min, or to 60 °C (140 °F) for 12 min. To protect against Salmonella infection, heating food for at least ten minutes at 75 °C (167 °F) is recommended, so the centre of the food reaches this temperature.
Initially, each Salmonella “species” was named according to clinical considerations, e.g., Salmonella typhi-murium (mouse typhoid fever), (Tindall et al.,2005) S. cholerae-suis. After it was recognized that host specificity did not exist for many species, new strains (or serovars, short for serological variants) received species names according to the location at which the new strain was isolated. Later, molecular findings led to the hypothesis that consisted of only one species, S. enterica, and the serovars were classified into six groups, two of which are medically relevant. As this now-formalized nomenclature is not in harmony with the traditional usage familiar to specialists in microbiology and infectologists, the traditional nomenclature is common. Currently, there are two recognized species: S. enterica, and S. bongori. In 2005 a third species, Salmonella subterranean, was thought to be added, but this has since been ruled out and is seen as another serovar. There are six main subspecies recognised: enterica (I), salamae (II), arizonae (IIIa), diarizonae (IIIb), houtenae (IV), and indica (VI). Historically, serotype (V) was bongori, which is now considered its own species.( Tindall et al.,2005)
The serovar, i.e., serotype, is a classification of Salmonella into subspecies based on antigens that the organism presents. It is based on the Kauffman-White classification scheme that differentiates serological varieties from each other. Serotypes are usually put into subspecies groups after the genus and species, with the serovars/serotypes capitalized, but not italicized: An example is Salmonella enterica serovar Typhimurium. More modern approaches for typing and subtyping Salmonella include DNA-based methods such as pulsed field gel electrophoresis (PFGE), Multiple Loci VNTR Analysis (MLVA), Multilocus sequence typing (MLST) and multiplex-PCR-based methods.
Salmonella as pathogens
Salmonella species are facultative intracellular pathogens. Many infections are due to ingestion of contaminated food. They can be divided into two groups—typhoidal and nontyphoidal Salmonella serovars. Nontyphoidal serovars are more common, and usually cause self-limiting gastrointestinal disease. They can infect a range of animals, and are zoonotic, meaning they can be transferred between humans and other animals. Typhoidal serovars include Salmonella Typhi and Salmonella Paratyphi A, which are adapted to humans and do not occur in other animals.
Infection with nontyphoidal serovars of Salmonella will generally result in food poisoning. Infection usually occurs when a person ingests foods that contain a high concentration of the bacteria. Infants and young children are much more susceptible to infection, easily achieved by ingesting a small number of bacteria. In infants, infection through inhalation of bacteria-laden dust is possible.
The organism enters through the digestive tract and must be ingested in large numbers to cause disease in healthy adults. An infectious process can only begin after living salmonellae (not only their toxins) reach the gastrointestinal tract. Some of the microorganisms are killed in the stomach, while the surviving salmonellae enter the small intestine and multiply in tissues (localized form). Gastric acidity is responsible for the destruction of the majority of ingested bacteria, however Salmonella has evolved a degree of tolerance to acidic environments that allows a subset of ingested bacteria to survive. Bacterial colonies may also become trapped in mucus produced in the oesophagus. By the end of the incubation period, the nearby cells are poisoned by endotoxins released from the dead salmonellae. The local response to the endotoxins is enteritis and gastrointestinal disorder (Porwollik 2011).
Invasive non-typhoidal salmonella disease
While in developed countries, nontyphoidal serovars present mostly as gastrointestinal disease, in sub-Saharan Africa these serovars create a major problem in bloodstream infections, and are the most commonly isolated bacteria from the blood of those presenting with fever. Bloodstream infections caused by nontyphoidal salmonellae in Africa were reported in 2012 to have a case fatality rate of 20–25%. Most cases of invasive nontyphoidal salmonella infection (iNTS) are caused by S Typhimurium or S Enteritidis. A new form of Salmonella Typhimurium (ST313) emerged in the southeast of the continent 75 years ago, followed by a second wave, which came out of central Africa 18 years later. The second wave of iNTS possibly originated in the Congo Basin, and early in the event picked up a gene making it resistant to the antibiotic chloramphenicol. This created the need to use expensive antimicrobial drugs in areas of Africa that were very poor, thus making treatment difficult. The variant is the cause of an enigmatic disease in sub-Saharan Africa called invasive non-typhoidal salmonella (iNTS), which affects Africa far more than other continents. This is thought to be due to the large proportion of the population with some degree of immune suppression or impairment due to the burden of HIV, malaria and malnutrition, especially in children. Its genetic makeup is evolving into a more typhoid-like bacteria, able to efficiently spread around the human body. Symptoms are reported to be diverse, including fever, hepatosplenomegaly, and respiratory symptoms, often with an absence of gastrointestinal symptoms.
Typhoid fever and Paratyphoid fever
Typhoid fever is caused by Salmonella serotypes which are strictly adapted to humans or higher primates—these include Salmonella Typhi, Paratyphi A, Paratyphi B and Paratyphi C. In the systemic form of the disease, salmonellae pass through the lymphatic system of the intestine into the blood of the patients (typhoid form) and are carried to various organs (liver, spleen, kidneys) to form secondary foci (septic form). Endotoxins first act on the vascular and nervous apparatus, resulting in increased permeability and decreased tone of the vessels, upset thermal regulation, vomiting and diarrhea. In severe forms of the disease, enough liquid and electrolytes are lost to upset the water-salt metabolism, decrease the circulating blood volume and arterial pressure, and cause hypovolemic shock. Septic shock may also develop. Shock of mixed character (with signs of both hypovolemic and septic shock) are more common in severe salmonellosis. Oliguria and azotemia develop in severe cases as a result of renal involvement due to hypoxia and toxemia.
In Germany, food poisoning infections must be reported. Between 1990 and 2005, the number of officially recorded cases decreased from approximately 200,000 to approximately 50,000 cases. In the United States, about 50,000 cases of Salmonella infection are reported each year. According to the World Health Organization, over 16 million people worldwide are infected with typhoid fever each year, with 500,000 to 600,000 fatal cases.
Molecular mechanisms of infection
Mechanisms of infection differ between typhoidal and nontyphoidal serovars, owing to their different targets in the body and the different symptoms that they cause. Both groups must enter by crossing the barrier created by the intestinal cell wall, but once they have passed this barrier they use different strategies to cause infection.
Nontyphoidal serovars preferentially enter M cells on the intestinal wall by bacterial-mediated endocytosis, a process associated with intestinal inflammation and diarrhoea. They are also able to disrupt tight junctions between the cells of the intestinal wall, impairing their ability to stop the flow of ions, water and immune cells into and out of the intestine. The combination of the inflammation caused by bacterial-mediated endocytosis and the disruption of tight junctions is thought to contribute significantly to the induction of diarrhoea.
Salmonellae are also able to breach the intestinal barrier via phagocytosis and trafficking by CD18-positive immune cells, which may be a mechanism key to typhoidal Salmonella infection. This is thought to be a more stealthy way of passing the intestinal barrier, and may therefore contribute to the fact that lower numbers of typhoidal Salmonella are required for infection than nontyphoidal Salmonella. Salmonella are able to enter macrophages via macropinocytosis. Typhoidal serovars can use this to achieve dissemination throughout the body via the mononuclear phagocyte system, a network of connective tissue that contains immune cells, and surrounds tissue associated with the immune system throughout the body.
Much of the success of Salmonella in causing infection is attributed to two type three secretion systems which function at different times during infection. One is required for the invasion of non-phagocytic cells, colonization of the intestine and induction of intestinal inflammatory responses and diarrhoea. The other is important for survival in macrophages and establishment of systemic disease. These systems contain many genes which must work co-operatively to achieve infection.
The AvrA toxin injected by the SPI1 type three secretion system of Salmonella Typhimurium works to inhibit the innate immune system by virtue of its serine/threonine acetyltransferase activity, and requires binding to eukaryotic target cell phytic acid (IP6). This leaves the host more susceptible to infection. In a 2011 paper, Yale University School of Medicine researchers described in detail how Salmonella is able to make these proteins line up in just the right sequence to invade host cells. “These mechanisms present us with novel targets that might form the basis for the development of an entirely new class of antimicrobials,” said Professor Dr. Jorge Galan, senior author of the paper and the Lucille P. Markey Professor of Microbial Pathogenesis and chair of the Section of Microbial Pathogenesis at Yale. In the new National Institutes of Health-funded study, Galan and colleagues identify what they call a bacterial sorting platform, which attracts needed proteins and lines them up in a specific order. If the proteins do not line up properly, Salmonella, as well as many other bacterial pathogens, cannot “inject” them into host cells to commandeer host cell functions, the lab has found. Understanding how this machine works raises the possibility of new therapies that disable this protein delivery machine, thwarting the ability of the bacterium to become pathogenic. The process would not kill the bacteria as most antibiotics do, but would cripple its ability to do harm. In theory, this means bacteria such as Salmonella might not develop resistance to new therapies as quickly as they usually do to conventional antibiotics.
Host Adaptation in Salmonella
Salmonella enterica, through some of its serovars, such as Typhimurium and S. Enteriditis, shows signs of not being limited to one host but has the ability to infect several different mammalian host species while other serovars such as, Typhi seem to be restricted to only a few hosts. Some of the ways that Salmonella through its serovars has adapted to its hosts is through the loss of genetic material and mutation. In more complex mammalian species, immune systems, which include pathogen specific immune responses, target serovars of Salmonella through binding of antibodies to structures like flagella. Through the loss of the genetic material that codes for a flagellum to form, Salmonella can evade a host’s immune system. In the study by more pathogenic serovars of S. enterica were found to have certain adhesins in common that have developed out of convergent evolution.This means that, as these strains of Salmonella have been exposed to similar conditions such as immune systems, similar structures evolved separately to complement these similar, more advanced defenses in hosts. There are still many questions about the way that Salmonella has evolved into so many different types but it has been suggested that Salmonella evolved through several phases. As have proffered, Salmonella most likely evolved through horizontal gene transfer, formation of new serovars due to additional pathogenicity islands and through an approximation of its ancestry. So, Salmonella could have evolved into its many different serovars through gaining genetic information from different pathogenic bacteria, and through this, different serovars emerged. The presence of several pathogenicity islands in the genome of different serovars have lent credence to viability of this postulation. Vaccine status( Porwollik 2011)
There is an urgency to develop an effective salmonella vaccine because of the recent outbreaks in Africa of antibiotic-resistant strains of the food-borne bacteria that are killing hundreds of thousands of people there, as well as the heavy annual worldwide death toll each year. Researchers say they have paved the way toward an effective Salmonella vaccine by identifying eight antigenic molecules from human and mouse infections. These antigens provide the research community with a foundation for developing a protective salmonella vaccine. A recent study has tested a vaccine on chickens which offered efficient protection against salmonellosis.
Pathogenic microorganisms found on door handle of convenices e.g. bacteria such as Staphylococcus spp Klebsillia, Escherichia coli, Pseudomonas aerogenosa. shigella, Salmonella spp are responsible for large number of diseases of man (Craig, 1997). Table 1shows the various bacteria present on door handles of conveniences. These bacteria are present due to the contamination of the handles by various activities done in the toilet; dumping of menstrual material, etc.
Door handles can sometimes be moist and thus provide a good surface for bacterial growth. They provide favorable conditions such as substrate acquired from human body and due to handling as well as dust from the environment. Most of the bacteria encountered in this study are members of the human flora. This suggests that humans are the major source of bacteria on the handles. The skin habours a complex ecosystem of microorganisms, which could be transient or resident (Nester et al., 2004). The number of bacteria on the skin surface ranges from 103 cfu/cm2 in dry areas to more than 107cfu/cm2 in moist areas (Brock et al., 1994; Willey et al., 2008). Colonization of the handles can also occur due to practice using water to clean the anus after using the toilet.(Galvani, 1974). These bacteria could have been introduced via contaminated water used in washing the anus.
S. aureus are usually harmless but are often able to cause infections (pyogenic infections) once they gain entry into damaged skin or deeper body tissues. It is also associated with peeling of superficial skin layer (exfoliation), impetigo, carbuncles and food intoxication (Brock et al., 1994; Jensen et al., 1997). It can be easily transferred from formites to person and initiate infections.
5.2 Conclusion and Recommendation
This study revealed that door handles can be contaminated with pathogenic microorganisms that are capable of causing diseases and infections. In order to reduce the level of contamination and exposure of individuals to infectious pathogens, it is important that door handles be handled with proper hygiene. Wash hand properly with detergent after using the convenience and the use of the hand sanitizer should be encouraged among the general populace. All the students within and outside presco campus should be enlightened on the use of hand sanitizer after opening the convenince. Some of the hand sanitizers were resisted by the isolates due to poor manufacturing therefore the government and health institutes (NAFDAC) should see to the proper manufacturing of the hand sanizeters and should help in teaching the public the dangers associated with poor personal hygiene.
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