Pseudomonas aeruginosa - wikipedia Pseudomonas aeruginosa Pseudomonas aeruginosa P. aeruginosa colony ( right ) and Staph. aureus colony ( left ) on trypticase soy agar Scientific classification Domain : Bacteria Phylum : Proteobacteria Class : Gammaproteobacteria Order : Pseudomonadales Family : Pseudomonadaceae Genus : Pseudomonas Species : P. aeruginosa Binomial name Pseudomonas aeruginosa ( Schröter 1872 ) Migula 1900 Synonyms Bacterium aeruginosum Schroeter 1872 Bacterium aeruginosum Cohn 1872 Micrococcus pyocyaneus Zopf 1884 Bacillus aeruginosus ( Schroeter 1872 ) Trevisan 1885 Bacillus pyocyaneus ( Zopf 1884 ) Flügge 1886 Pseudomonas pyocyanea ( Zopf 1884 ) Migula 1895 Bacterium pyocyaneum ( Zopf 1884 ) Lehmann and Neumann 1896 Pseudomonas polycolor Clara 1930 Pseudomonas vendrelli nomen nudum 1938 Pseudomonas aeruginosa is a common Gram - negative, rod - shaped bacterium that can cause disease in plants and animals, including humans. A species of considerable medical importance, P. aeruginosa is a multidrug resistant pathogen recognized for its ubiquity, its intrinsically advanced antibiotic resistance mechanisms, and its association with serious illnesses -- hospital - acquired infections such as ventilator - associated pneumonia and various sepsis syndromes. The organism is considered opportunistic insofar as serious infection often occurs during existing diseases or conditions -- most notably cystic fibrosis and traumatic burns. It is also found generally in the immunocompromised but can infect the immunocompetent as in hot tub folliculitis. Treatment of P. aeruginosa infections can be difficult due to its natural resistance to antibiotics. When more advanced antibiotic drug regimens are needed adverse effects may result. It is citrate, catalase, and oxidase positive. It is found in soil, water, skin flora, and most man - made environments throughout the world. It thrives not only in normal atmospheres, but also in low - oxygen atmospheres, thus has colonized many natural and artificial environments. It uses a wide range of organic material for food ; in animals, its versatility enables the organism to infect damaged tissues or those with reduced immunity. The symptoms of such infections are generalized inflammation and sepsis. If such colonizations occur in critical body organs, such as the lungs, the urinary tract, and kidneys, the results can be fatal. Because it thrives on moist surfaces, this bacterium is also found on and in medical equipment, including catheters, causing cross-infections in hospitals and clinics. It is also able to decompose hydrocarbons and has been used to break down tarballs and oil from oil spills. P. aeruginosa is not extremely virulent in comparison with other major pathogenic bacterial species -- for example Staphylococcus aureus and Streptococcus pyogenes -- though P. aeruginosa is capable of extensive colonization, and can aggregate into enduring biofilms. Contents 1 Nomenclature 2 Biology 2.1 Genome 2.2 Metabolism 2.3 Cellular cooperation 3 Pathogenesis 3.1 Toxins 3.2 Phenazines 3.3 Triggers 3.4 Plants and invertebrates 3.5 Quorum sensing 3.6 Biofilms and treatment resistance 4 Diagnosis 4.1 Identification 5 Treatment 5.1 Antibiotic resistance 5.2 Prevention 5.3 Experimental therapies 6 Research 7 See also 8 References 9 External links Nomenclature A culture dish with Pseudomonas The word Pseudomonas means `` false unit '', from the Greek pseudēs ( Greek : ψευδής, false ) and ( Latin : monas, from Greek : μονάς, a single unit ). The stem word mon was used early in the history of microbiology to refer to germs, e.g., kingdom Monera. The species name aeruginosa is a Latin word meaning verdigris ( `` copper rust '' ), referring to the blue - green color of laboratory cultures of the species. This blue - green pigment is a combination of two metabolites of P. aeruginosa, pyocyanin ( blue ) and pyoverdine ( green ), which impart the blue - green characteristic color of cultures. Another assertion is that the word may be derived from the Greek prefix ae - meaning `` old or aged '', and the suffix ruginosa means wrinkled or bumpy. The names pyocyanin and pyoverdine are from the Greek, with pyo -, meaning `` pus '', cyanin, meaning `` blue '', and verdine, meaning `` green ''. Pyoverdine in the absence of pyocyanin is a fluorescent - yellow color. Gram - stained P. aeruginosa bacteria ( pink - red rods ) Biology Genome The genome of P. aeruginosa is relatively large ( 5.5 -- 6.8 Mb ) and encodes between 5,500 and 6,000 open reading frames, depending on the strain ; Comparison of 389 genomes from different P. aeruginosa strains showed that just 17.5 % is shared. This part of the genome is the P. aeruginosa core genome. strain : VRFPA04 C3719 PAO1 PA14 PACS2 genome size ( bp ) 6,818,030 6,222,097 6,264,404 6,537,648 6,492,423 ORFs 5,939 5,578 5,571 5,905 5,676 Metabolism P. aeruginosa is a facultative anaerobe, as it is well adapted to proliferate in conditions of partial or total oxygen depletion. This organism can achieve anaerobic growth with nitrate or nitrite as a terminal electron acceptor. When oxygen, nitrate, and nitrite are absent, it is able to ferment arginine and pyruvate by substrate - level phosphorylation. Adaptation to microaerobic or anaerobic environments is essential for certain lifestyles of P. aeruginosa, for example, during lung infection in cystic fibrosis and primary ciliary dyskinesia, where thick layers of lung mucus and alginate surrounding mucoid bacterial cells can limit the diffusion of oxygen. P. aeruginosa growth within the human body can be asymptomatic until the bacteria form a biofilm, which overwhelms the immune system. These biofilms are found in the lungs of people with cystic fibrosis and primary ciliary dyskinesia, and can prove fatal. Cellular cooperation P. aeruginosa relies on iron as a nutrient source to grow. However, iron is not easily accessible because it is not commonly found in the environment. Iron is usually found in a largely insoluble ferric form. Furthermore, excessively high levels of iron can be toxic to P. aeruginosa. To overcome this and regulate proper intake of iron, P. aeruginosa uses siderophores, which are secreted molecules that bind and transport iron. These iron - siderophore complexes, however, are not specific. The bacterium that produced the siderophores does not necessarily receive the direct benefit of iron intake. Rather, all members of the cellular population are equally likely to access the iron - siderophore complexes. Members of the cellular population that can efficiently produce these siderophores are commonly referred to as cooperators ; members that produce little to no siderophores are often referred to as cheaters. Research has shown when cooperators and cheaters are grown together, cooperators have a decrease in fitness, while cheaters have an increase in fitness. The magnitude of change in fitness increases with increasing iron limitation. With an increase in fitness, the cheaters can outcompete the cooperators ; this leads to an overall decrease in fitness of the group, due to lack of sufficient siderophore production. These observations suggest that having a mix of cooperators and cheaters can reduce the virulent nature of P. aeruginosa. Pathogenesis Phagocytosis of P. aeruginosa by neutrophil in patient with bloodstream infection ( Gram stain ) An opportunistic, nosocomial pathogen of immunocompromised individuals, P. aeruginosa typically infects the airway, urinary tract, burns, and wounds, and also causes other blood infections. Infections Details and common associations High - risk groups Pneumonia Diffuse bronchopneumonia Cystic fibrosis patients Septic shock Associated with a purple - black skin lesion ecthyma gangrenosum Neutropenic patients Urinary tract infection Urinary tract catheterization Gastrointestinal infection Necrotising enterocolitis Premature infants and neutropenic cancer patients Skin and soft tissue infections Hemorrhage and necrosis People with burns or wound infections It is the most common cause of infections of burn injuries and of the outer ear ( otitis externa ), and is the most frequent colonizer of medical devices ( e.g., catheters ). Pseudomonas can be spread by equipment that gets contaminated and is not properly cleaned or on the hands of healthcare workers. Pseudomonas can, in rare circumstances, cause community - acquired pneumonias, as well as ventilator - associated pneumonias, being one of the most common agents isolated in several studies. Pyocyanin is a virulence factor of the bacteria and has been known to cause death in C. elegans by oxidative stress. However, salicylic acid can inhibit pyocyanin production. One in ten hospital - acquired infections is from Pseudomonas. Cystic fibrosis patients are also predisposed to P. aeruginosa infection of the lungs. P. aeruginosa may also be a common cause of `` hot - tub rash '' ( dermatitis ), caused by lack of proper, periodic attention to water quality. Since these bacteria like moist environments, such as hot tubs and swimming pools, they can cause skin rash or swimmer 's ear. Pseudomonas is also a common cause of postoperative infection in radial keratotomy surgery patients. The organism is also associated with the skin lesion ecthyma gangrenosum. P. aeruginosa is frequently associated with osteomyelitis involving puncture wounds of the foot, believed to result from direct inoculation with P. aeruginosa via the foam padding found in tennis shoes, with diabetic patients at a higher risk. Toxins P. aeruginosa uses the virulence factor exotoxin A to inactivate eukaryotic elongation factor 2 via ADP - ribosylation in the host cell, much as the diphtheria toxin does. Without elongation factor 2, eukaryotic cells can not synthesize proteins and necrotise. The release of intracellular contents induces an immunologic response in immunocompetent patients. In addition P. aeruginosa uses an exoenzyme, ExoU, which degrades the plasma membrane of eukaryotic cells, leading to lysis. Increasingly, it is becoming recognized that the iron - acquiring siderophore, pyoverdine, also functions as a toxin by removing iron from mitochondria, inflicting damage on this organelle. Phenazines Phenazines are redox - active pigments produced by P. aeruginosa. These pigments are involved in quorum sensing, virulence, and iron acquisition. P. aeruginosa produces several pigments all produced by a biosynthetic pathway : pyocyanin, 1 - hydroxyphenazine, phenazine - 1 - carboxamide, 5 - methylphenazine - 1 - carboxylic acid betaine, and aeruginosin A. Two operons are involved in phenazine biosynthesis : phzA1B1C1D1E1F1G1 and phzA2B2C2D2E2F2G2. These operons convert a chorismic acid to the phenazines mentioned above. Three key genes, phzH, phzM, and phzS convert phenazine - 1 - carboxylic acid to the phenazines mentioned above. Though phenazine biosynthesis is well studied, questions remain as to the final structure of the brown phenazine pyomelanin. When pyocyanin biosynthesis is inhibited, a decrease in P. aeruginosa pathogenicity is observed in vitro. This suggests that pyocyanin is most responsible for the initial colonization of P. aeruginosa in vivo. Triggers With low phosphate levels, P. aeruginosa has been found to activate from benign symbiont to express lethal toxins inside the intestinal tract and severely damage or kill the host, which can be mitigated by providing excess phosphate instead of antibiotics. Plants and invertebrates In higher plants, P. aeruginosa induces soft rot, for example in Arabidopsis thaliana ( Thale cress ) and Lactuca sativa ( lettuce ). It is also pathogenic to invertebrate animals, including the nematode Caenorhabditis elegans, the fruit fly Drosophila and the moth Galleria mellonella. The associations of virulence factors are the same for plant and animal infections. Quorum sensing Regulation of gene expression can occur through cell - cell communication or quorum sensing ( QS ) via the production of small molecules called autoinducers. The extracellular accumulation of these molecules signals to bacteria to alter gene expression and coordinate behavior. P. aeruginosa employs three interconnected QS systems -- lasRl, rhlRl, and PQS -- that each produce unique signaling molecules. Detection of these molecules indicates P. aeruginosa is growing as biofilm within the lungs of cystic fibrosis patients. QS is known to control expression of a number of virulence factors, including the pigment pyocyanin. Another form of gene regulation that allows the bacteria to rapidly adapt to surrounding changes is through environmental signaling. Recent studies have discovered anaerobiosis can significantly impact the major regulatory circuit of QS. This important link between QS and anaerobiosis has a significant impact on production of virulence factors of this organism. Garlic experimentally blocks quorum sensing in P. aeruginosa. Biofilms and treatment resistance Biofilms of P. aeruginosa can cause chronic opportunistic infections, which are a serious problem for medical care in industrialized societies, especially for immunocompromised patients and the elderly. They often can not be treated effectively with traditional antibiotic therapy. Biofilms seem to protect these bacteria from adverse environmental factors. P. aeruginosa can cause nosocomial infections and is considered a model organism for the study of antibiotic - resistant bacteria. Researchers consider it important to learn more about the molecular mechanisms that cause the switch from planktonic growth to a biofilm phenotype and about the role of QS in treatment - resistant bacteria such as P. aeruginosa. This should contribute to better clinical management of chronically infected patients, and should lead to the development of new drugs. Many genes and factors affect biofilm formation in P. aeruginosa. One of the main gene operons responsible for the initiation and maintaining the biofilm is the PSL operon. This 15 - gene operon is responsible for the cell - cell and cell - surface interactions required for cell communication. It is also responsible for the sequestering of the extracellular polymeric substance matrix. This matrix is composed of nucleic acids, amino acids, carbohydrates, and various ions. This matrix is one of the main resistance mechanisms in the biofilms of P. aeruginosa. Cyclic di - GMP is a major contributor to biofilm adherent properties. This signalling molecule in high quantities makes superadherent biofilms. When suppressed, the biofilms are less adherent and easier to treat. Polysaccharide synthesis locus ( PSL ) and cdi - GMP form a positive feedback loop. PSL stimulates cdi - GMP production, while high cd - GMP turns on the operon and increases activity of the operon. Recent studies have shown that the dispersed cells from P. aeruginosa biofilms have lower c - di - GMP levels and different physiologies from those of planktonic and biofilm cells. Such dispersed cells are found to be highly virulent against macrophages and C. elegans, but highly sensitive towards iron stress, as compared with planktonic cells. Recently, scientists have been examining the possible genetic basis for P. aeruginosa resistance to antibiotics such as tobramycin. One locus identified as being an important genetic determinant of the resistance in this species is ndvB, which encodes periplasmic glucans that may interact with antibiotics and cause them to become sequestered into the periplasm. These results suggest a genetic basis exists behind bacterial antibiotic resistance, rather than the biofilm simply acting as a diffusion barrier to the antibiotic. Diagnosis Production of pyocyanin, water - soluble green pigment of P. aeruginosa ( left tube ) Depending on the nature of infection, an appropriate specimen is collected and sent to a bacteriology laboratory for identification. As with most bacteriological specimens, a Gram stain is performed, which may show Gram - negative rods and / or white blood cells. P. aeruginosa produces colonies with a characteristic `` grape - like '' or `` fresh - tortilla '' odor on bacteriological media. In mixed cultures, it can be isolated as clear colonies on MacConkey agar ( as it does not ferment lactose ) which will test positive for oxidase. Confirmatory tests include production of the blue - green pigment pyocyanin on cetrimide agar and growth at 42 ° C. A TSI slant is often used to distinguish nonfermenting Pseudomonas species from enteric pathogens in faecal specimens. When P. aeruginosa is isolated from a normally sterile site ( blood, bone, deep collections ), it is generally considered dangerous, and almost always requires treatment. However, P. aeruginosa is frequently isolated from nonsterile sites ( mouth swabs, sputum, etc. ), and, under these circumstances, it may represent colonization and not infection. The isolation of P. aeruginosa from nonsterile specimens should, therefore, be interpreted cautiously, and the advice of a microbiologist or infectious diseases physician / pharmacist should be sought prior to starting treatment. Often, no treatment is needed. Identification Test Results Gram Stain - Oxidase + Indole Production - Methyl Red - Voges - Proskaeur - Citrate + Hydrogen Sulfide Production - Urea Hydrolysis - Phenylalanine Deaminase - Lysine Decarboxylase - Motility + Gelatin Hydrolysis + Acid from lactose - acid from glucose + acid from maltose - acid from mannitol + acid from sucrose - nitrate reduction + DNAse - Lipase + Pigment + ( bluish green pigmentation ) Catalase + P. aeruginosa is a Gram - negative, aerobic ( and at times facultatively anaerobic ), bacillus with unipolar motility. It has been identified as an opportunistic pathogen of both humans and plants. P. aeruginosa is the type species of the genus Pseudomonas. In certain conditions, P. aeruginosa can secrete a variety of pigments, including pyocyanin ( blue ), pyoverdine ( yellow and fluorescent ), pyorubin ( red ), and pyomelanin ( brown ). These can be used to identify the organism. Pseudomonas aeruginosa fluorescence under UV illumination P. aeruginosa is often preliminarily identified by its pearlescent appearance. Clinical identification of P. aeruginosa may include identifying the production of both pyocyanin and fluorescein, as well as its ability to grow at 42 ° C. P. aeruginosa is capable of growth in diesel and jet fuels, where it is known as a hydrocarbon - using microorganism, causing microbial corrosion. It creates dark, gellish mats sometimes improperly called `` algae '' because of their appearance. Treatment Many P. aeruginosa isolates are resistant to a large range of antibiotics and may demonstrate additional resistance after unsuccessful treatment. It should usually be possible to guide treatment according to laboratory sensitivities, rather than choosing an antibiotic empirically. If antibiotics are started empirically, then every effort should be made to obtain cultures ( before administering first dose of antibiotic ), and the choice of antibiotic used should be reviewed when the culture results are available. The antibiogram of P. aeruginosa on Mueller - Hinton agar Due to widespread resistance to many common first - line antibiotics, carbapenems, polymyxins, and more recently tigecycline were considered to be the drugs of choice ; however, resistance to these drugs has also been reported. Despite this, they are still being used in areas where resistance has not yet been reported. Use of β - lactamase inhibitors such as sulbactam has been advised in combination with antibiotics to enhance antimicrobial action even in the presence of a certain level of resistance. Combination therapy after rigorous antimicrobial susceptibility testing has been found to be the best course of action in the treatment of multidrug - resistant P. aeruginosa. Some next - generation antibiotics that are reported as being active against P. aeruginosa include doripenem, ceftobiprole, and ceftaroline. However, these require more clinical trials for standardization. Therefore, research for the discovery of new antibiotics and drugs against P. aeruginosa is very much needed. Antibiotics that may have activity against P. aeruginosa include : aminoglycosides ( gentamicin, amikacin, tobramycin, but not kanamycin ) quinolones ( ciprofloxacin, levofloxacin, but not moxifloxacin ) cephalosporins ( ceftazidime, cefepime, cefoperazone, cefpirome, ceftobiprole, but not cefuroxime, cefotaxime, or ceftriaxone ) antipseudomonal penicillins : carboxypenicillins ( carbenicillin and ticarcillin ), and ureidopenicillins ( mezlocillin, azlocillin, and piperacillin ). P. aeruginosa is intrinsically resistant to all other penicillins. carbapenems ( meropenem, imipenem, doripenem, but not ertapenem ) polymyxins ( polymyxin B and colistin ) monobactams ( aztreonam ) As fluoroquinolone is one of the few antibiotics widely effective against P. aeruginosa, in some hospitals, its use is severely restricted to avoid the development of resistant strains. On the rare occasions where infection is superficial and limited ( for example, ear infections or nail infections ), topical gentamicin or colistin may be used. For pseudomonal wound infections, acetic acid with concentrations from 0.5 % to 5 % can be an effective bacteriostatic agent in eliminating the bacteria from the wound. Usually a sterile gauze soaked with acetic acid is placed on the wound after irrigation with normal saline. Dressing would be done once per day. Pseudomonas is usually eliminated in 90 % of the cases after 10 to 14 days of treatment. Antibiotic resistance One of the most worrisome characteristics of P. aeruginosa is its low antibiotic susceptibility, which is attributable to a concerted action of multidrug efflux pumps with chromosomally encoded antibiotic resistance genes ( e.g., mexAB, mexXY, etc. ) and the low permeability of the bacterial cellular envelopes. In addition to this 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, including 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 favors 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 antibiotics treatment. Mechanisms underlying antibiotic resistance have been found to include production of antibiotic - degrading or antibiotic - inactivating enzymes, outer membrane proteins to evict the antibiotics and mutations to change antibiotic targets. Presence of antibiotic - degrading enzymes such as extended - spectrum β - lactamases like PER - 1, PER - 2, VEB - 1, AmpC cephalosporinases, carbapenemases like serine oxacillinases, metallo - b - lactamases, OXA - type carbapenemases, aminoglycoside - modifying enzymes, among others have been reported. P. aeruginosa can also modify the targets of antibiotic action, for example methylation of 16S rRNA to prevent aminoglycoside binding and modification of DNA, or topoisomerase to protect it from the action of quinolones. P. aeruginosa has also been reported to possess multidrug efflux pumps like AdeABC and AdeDE efflux systems that confer resistance against number of antibiotic classes. An important factor found to be associated with antibiotic resistance is the decrease in the virulence capabilities of the resistant strain. Such findings have been reported in the case of rifampicin - resistant and colistin - resistant strains, in which decrease in infective ability, quorum sensing and motility have been documented. Mutations in DNA gyrase are commonly associated with antibiotic resistance in P. aeruginosa. These mutations, when combined with others, confer high resistance without hindering survival. Additionally, genes involved in cyclic - di - GMP signaling may contribute to resistance. When grown in vitro conditions designed to mimic a cystic fibrosis patient 's lungs, these genes mutate repeatedly. Two small RNA s : Sr0161 and ErsA were shown to interact with mRNA encoding the major porin OprD responsible for the uptake of carbapenem antibiotics into the periplasm. The sRNAs bind to the 5'UTR of oprD causing increase in bacterial resistance to meropenem. Another sRNA : Sr006 was suggested to positively regulate ( post-transcriptionally ) the expression of PagL, an enzyme responsible for deacylation of lipid A. This reduces the pro-inflammatory property of lipid A. Furthermore, similarly to study in Salmonella Sr006 regulation of PagL expression was suggested to aid in polymyxin B resistance. Prevention Probiotic prophylaxis may prevent colonization and delay onset of Pseudomonas infection in an ICU setting. Immunoprophylaxis against Pseudomonas is being investigated. The risk of contracting P. aeruginosa can be reduced by avoiding pools, hot tubs, and other bodies of standing water ; regularly disinfecting and / or replacing equipment that regularly encounters moisture ( such as contact lens equipment and solutions ) ; and washing one 's hands often ( which is protective against many other pathogens as well ). However, even the best hygiene practices can not totally protect an individual against P. aeruginosa, given how common P. aeruginosa is in the environment. Experimental therapies Phage therapy against P. aeruginosa has been investigated as a possible effective treatment, which can be combined with antibiotics, has no contraindications and minimal adverse effects. Phages are produced as sterile liquid, suitable for intake, applications etc. Phage therapy against ear infections caused by P. aeruginosa was reported in the journal Clinical Otolaryngology in August 2009. Research Last 2013, João Xavier described an experiment in which P. aeruginosa, when subjected to repeated rounds of conditions in which it needed to swarm to acquire food, developed the ability to `` hyperswarm '' at speeds 25 % faster than baseline organisms, by developing multiple flagella, whereas the baseline organism has a single flagellum. This result was notable in the field of experimental evolution in that it was highly repeatable. P. aeruginosa has been studied for use in bioremediation and use in processing polyethylene in municipal solid waste. See also Wikimedia Commons has media related to Pseudomonas aeruginosa. Bacteriological water analysis Contamination control Nosocomial infection NrsZ small RNA AsponA antisense RNA Repression of heat shock gene expression ( ROSE ) element Pseudomon - 1 RNA motif ( ErsA sRNA ) PrrF RNA Pseudomonas sRNA P16 ( RgsA sRNA ) References Jump up ^ Balcht A, Smith R ( 1994 ). Pseudomonas aeruginosa : Infections and Treatment. Informa Health Care. pp. 83 -- 84. ISBN 0 - 8247 - 9210 - 6. Jump up ^ Itah A, Essien J ( 2005 ). `` Growth Profile and Hydrocarbonoclastic Potential of Microorganisms Isolated from Tarballs in the Bight of Bonny, Nigeria ''. World Journal of Microbiology and Biotechnology. 21 ( 6 -- 7 ) : 1317 -- 22. doi : 10.1007 / s11274 - 004 - 6694 - z. 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External links Type strain of Pseudomonas aeruginosa at BacDive - the Bacterial Diversity Metadatabase Infectious diseases Bacterial disease : Proteobacterial G − primarily A00 -- A79, 001 -- 041, 080 -- 109 α Rickettsiales Rickettsiaceae / ( Rickettsioses ) Typhus Rickettsia typhi Murine typhus Rickettsia prowazekii Epidemic typhus, Brill -- Zinsser disease, Flying squirrel typhus Spotted fever Tick - borne Rickettsia rickettsii Rocky Mountain spotted fever Rickettsia conorii Boutonneuse fever Rickettsia japonica Japanese spotted fever Rickettsia sibirica North Asian tick typhus Rickettsia australis Queensland tick typhus Rickettsia honei Flinders Island spotted fever Rickettsia africae African tick bite fever Rickettsia parkeri American tick bite fever Rickettsia aeschlimannii Rickettsia aeschlimannii infection Mite - borne Rickettsia akari Rickettsialpox Orientia tsutsugamushi Scrub typhus Flea - borne Rickettsia felis Flea - borne spotted fever Anaplasmataceae Ehrlichiosis : Anaplasma phagocytophilum Human granulocytic anaplasmosis, Anaplasmosis Ehrlichia chaffeensis Human monocytotropic ehrlichiosis Ehrlichia ewingii Ehrlichiosis ewingii infection Rhizobiales Brucellaceae Brucella abortus Brucellosis Bartonellaceae Bartonellosis : Bartonella henselae Cat - scratch disease Bartonella quintana Trench fever Either B. henselae or B. quintana Bacillary angiomatosis Bartonella bacilliformis Carrion 's disease, Verruga peruana β Neisseriales M+ Neisseria meningitidis / meningococcus Meningococcal disease, Waterhouse -- Friderichsen syndrome, Meningococcal septicaemia M − Neisseria gonorrhoeae / gonococcus Gonorrhea ungrouped : Eikenella corrodens / Kingella kingae HACEK Chromobacterium violaceum Chromobacteriosis infection Burkholderiales Burkholderia pseudomallei Melioidosis Burkholderia mallei Glanders Burkholderia cepacia complex Bordetella pertussis / Bordetella parapertussis Pertussis γ Enterobacteriales ( OX − ) Lac+ Klebsiella pneumoniae Rhinoscleroma, Klebsiella pneumonia Klebsiella granulomatis Granuloma inguinale Klebsiella oxytoca Escherichia coli : Enterotoxigenic Enteroinvasive Enterohemorrhagic O157 : H7 O104 : H4 Hemolytic - uremic syndrome Enterobacter aerogenes / Enterobacter cloacae Slow / weak Serratia marcescens Serratia infection Citrobacter koseri / Citrobacter freundii Lac − H2S+ Salmonella enterica Typhoid fever, Paratyphoid fever, Salmonellosis H2S − Shigella dysenteriae / sonnei / flexneri / boydii Shigellosis, Bacillary dysentery Proteus mirabilis / Proteus vulgaris Yersinia pestis Plague / Bubonic plague Yersinia enterocolitica Yersiniosis Yersinia pseudotuberculosis Far East scarlet - like fever Pasteurellales Haemophilus : H. influenzae Haemophilus meningitis Brazilian purpuric fever H. ducreyi Chancroid H. parainfluenzae HACEK Pasteurella multocida Pasteurellosis Actinobacillus Actinobacillosis Aggregatibacter actinomycetemcomitans HACEK Legionellales Legionella pneumophila / Legionella longbeachae Legionnaires ' disease Coxiella burnetii Q fever Thiotrichales Francisella tularensis Tularemia Vibrionaceae Vibrio cholerae Cholera Vibrio vulnificus Vibrio parahaemolyticus Vibrio alginolyticus Plesiomonas shigelloides Pseudomonadales Pseudomonas aeruginosa Pseudomonas infection Moraxella catarrhalis Acinetobacter baumannii Xanthomonadaceae Stenotrophomonas maltophilia Cardiobacteriaceae Cardiobacterium hominis HACEK Aeromonadales Aeromonas hydrophila / Aeromonas veronii Aeromonas infection ε Campylobacterales Campylobacter jejuni Campylobacteriosis, Guillain -- Barré syndrome Helicobacter pylori Peptic ulcer, MALT lymphoma, Gastric cancer Helicobacter cinaedi Helicobacter cellulitis Taxon identifiers Wikidata : Q31856 Wikispecies : Pseudomonas aeruginosa BacDive : 12800 EoL : 973051 EPPO : PSDMAE GBIF : 3223154 IRMNG : 10843791 ITIS : 965278 NCBI : 287 NZOR : a74e3123 - 4581 - 4ac3 - a203 - 69199188cbd3 NDL : 00569851 Biology portal Retrieved from `` https://en.wikipedia.org/w/index.php?title=Pseudomonas_aeruginosa&oldid=854140981 '' Categories : Antibiotic - resistant bacteria Gram - negative bacteria Pseudomonadales Bacteria described in 1872 Hidden categories : Articles with ' species ' microformats Articles containing Latin - language text All articles with unsourced statements Articles with unsourced statements from May 2018 Articles with unsourced statements from May 2010 Articles with unsourced statements from March 2011 Wikipedia articles with NDL identifiers Talk Contents About Wikipedia Wikispecies Català Čeština Deutsch Eesti Ελληνικά Español Euskara فارسی Français Galego Bahasa Indonesia Italiano עברית Latina Latviešu Nederlands 日本 語 Polski Português Română Русский Shqip Simple English Suomi Svenska ไทย Türkçe Українська Tiếng Việt 中文 22 more Edit links This page was last edited on 9 August 2018, at 07 : 08 ( UTC ). 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Question: despite all its virulence factors what type of pathogen is pseudomonas aeruginosa
Answer: multidrug resistant pathogen