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Pseudomonas and Related Organisms Pseudomonas and related organisms Aerobic gram-negative nonfermentative rods Pseudomonas aeruginosa: opportunistic infections of multiple sites Burkholderia cepacia: RT infection in cystic fibrosis patients, UTI, opportunistic infections Burkholderia pseudomallei: opportunistic pulmonary infections or sepsis Stenotrophomonas maltophilia: opportunistic infections Acinetobacter baumannii: opportunistic infections of RT Moraxella catarrhalis: opportunistic RT infections Pseudomonas Structure and Physiology Gram-negative rods. Motile with polar flagella. Obligate aerobe. Oxidase-positive. Do not ferment carbohydrates. Resistant to multiple drugs. P. aeruginosa Forms round colonies with a fluorescent greenish color, sweet odor, and -hemolysis. Pyocyanin- nonfluorescent bluish pigment; pyoverdin- fluorescent greenish pigment; pyorubin, and pyomelanin Some strains have a prominent capsule (alginate). Identification of P. aeruginosa is usually based on oxidase test and its colonial morphology: -hemolysis, the presence of characteristic pigments and sweet odor, and growth at 42 oC. P. aeruginosa Pathogenesis and Immunity This organism is widely distributed in nature and is commonly present in moist environments in hospitals. It is pathogenic only when introduced into areas devoid of normal defenses, e.g., 1. Disruption of mucous membrane and skin. 2. Usage of intravenous or urinary catheters. 3. Neutropenia (as in cancer therapy). P. aeruginosa can infect almost any external site or organ. P. aeruginosa is invasive and toxigenic. It attaches to and colonizes the mucous membrane or skin, invade locally, and produces systemic diseases and septicemia. P. aeruginosa is resistant to many antibiotics. It becomes dominant when more susceptible bacteria of the normal flora are suppressed. P. aeruginosa Pathogenesis Antigenic structure, Proteases enzymes, and toxins Serine protease, Pili and nonpilus adhesins. metalloprotease and alkaline Capsule (alginate, glycocalyx): protease cause tissue seen in cultures from patients damage and help bacteria with cystic fibrosis. spread LPS- endotoxin, multiple Phospholipase C: a hemolysin immunotypes. Exotoxin A: causes tissue Pyocyanin: catalyzes necrosis and is lethal for animals production of toxic forms of (disrupts protein synthesis); oxygen that cause tissue immunosuppressive. damage. It also induces IL-8 production. Pyoverdin: a Exoenzyme S and T: cytotoxic to siderophore. host cells. P. aeruginosa Clinical Diseases Infection of wounds and burns Ear infections (blue-green pus). Patients with Otitis externa: mild in severe burns may develop into swimmers; malignant (invasive) bacteriemia. in diabetic patients. Skin and nail infections Chronic otitis media Meningitis (when introduced by lumbar puncture). Osteochondritis of the foot. Pulmonary infection Urinary tract infection Tracheobronchitis Sepsis: most cases originate Necrotizing pneumonia in CF from infections of lower RT, UT, patients: diffuse, bilateral and skin and soft tissue. bronchopneumonia with Ecthyma gangrenosum microabscess and necrosis. (hemorrhagic necrosis of skin Eye infections: corneal ulcer. may be seen in some patients. P. aeruginosa Laboratory Diagnosis Specimen: skin lesions, pus, urine, blood, spinal fluid, sputum. Culture: blood agar plate and differential media. Identification of P. aeruginosa is described above. Several subtyping methods, including phage typing and molecular typing, are available for epidemiologic purposes. Treatment Combined antibiotic therapy is generally required to avoid resistance that develops rapidly when single drugs are employed. Avoid using inappropriate broad-spectrum antibiotics, which can suppress the normal flora and permit overgrowth of resistant pseudomonads. P. aeruginosa Prevention and Control Pseudomonas spp. normally inhabit soil, water, and vegetation and can be isolated from the skin, throat, and stool of healthy persons. Spread is via contact with fomites or by ingestion of contaminated food and water. High risk population: patients receiving broad-spectrum antibiotics, with leukemia, burns, cystic fibrosis, and immunosuppression. Methods for control of infection are similar to those for other nosocomial pathogens. Special attention should be paid to sinks, water baths, showers, hot tubs, and other wet areas. P. aeruginosa Prevention and Control Control: 1. Patients at high risk should not be admitted to a ward where cases of pseudomonas infection are present. 2. Patients infected with P. aeruginosa should be isolated. 3. Sterilize all instruments, apparatus, and dressing; antimicrobial and other therapeutic substances. 4. Monitor clinically relevant isolates of P. aeruginosa by a suitable typing system to identify epidemic strains. Stenotrophomonas maltophilia A common nonfermentative, gram-negative isolate. It infects debilitated or immunocompromised persons, and causes a wide spectrum of diseases, including wound infections, UT infections, pneumonia, sepsis, meningitis, etc. It is resistant to many commonly used antibiotics, and patients receiving long-term antibiotic therapy are particularly at risk for acquiring infections. Infections may be acquired from iv catheters, contaminated disinfectants, respiratory therapy and monitoring equipment, and ice machines. Burkholderia They colonize the moist environmental surfaces and are commonly associated with nosocomial infections. B. cepacia complex (of 9 species), B. gladioli and B. pseudomallei are important pathogens. B. cepacia complex causes RT infections particularly in cystic fibrosis patients, UT infections and septicemia. Usually non-fatal except for RT infections in CF patients. B. pseudomallei usually causes opportunistic infections (called melioidosis , but may sometimes infect previously healthy persons. Infection by this organism may result in asymptomatic infection, acute suppurative cutaneous infection, and chronic pulmonary infection ranging in severity from mild bronchitis to necrotizing pneumonia. All may progress to sepsis. 2005/7/30 台南高雄疑似發生類鼻疽疫情，疾病管制局提 醒民眾，皮膚如有傷口，請勿接觸污染的土壤或水源 疾病管制局今天公佈今年自七月11日至29日以來，類鼻疽累計通 報16例，其中高雄縣9例、台南市4例、高雄市2例、台南縣1例。 其中6例死亡，3例在加護病房，另7例住普通病房。類鼻疽係由 類鼻疽伯克氏菌Burkholderia pseudomallei所造成的臨床感染 症，屬假單孢菌屬革蘭氏陰性桿菌，此菌在土壤、水池及積水環 境中存在，會感染馬、羊、豬等動物以及人類。其流行地域為東 南亞地區及澳洲北部的熱帶地域。該局自89年即將此病納入監測。 89年通報病例1例、90年15例、91年9例、92年5例、93年13例。 本次疫情發生原因，疾病管制局初步調查研判可能係因日前南部 豪大雨，將土壤中之病菌沖刷出來，所造成的民眾感染事件，病 例多發生在二仁溪流域。該局鄭重呼籲在二仁溪流域附近居民， 若有發燒等症狀者，務必迅速就醫。並告訴醫師居住地區，疾病 管制局呼籲，醫師對於上述地區發燒病患，應先排除感染此病的 可能性，若有懷疑應立即以抗生素治療，並採檢送驗。 Corynebacterium C. diphtheriae: causes diphtheria. Other Corynebacterium spp. (> 100 species) and related genera (coryneform) may cause opportunistic infections. Gram-positive, irregularly-shaped rods. "Club shaped". Strains of this genus contain short mycolic acid in the cell wall. In stained smears, individual rods tend to lie parallel or at acute angles to one another (palisades). Metachromatic granules (often near the poles) give the rod a beaded appearance. Grow aerobically on most media. Corynebacteria grow on Löffler's serum medium more readily than other respiratory pathogens, and show typical morphology in smears. Non-motile; noncapsulate. C. diphtheriae Pathogenesis and Immunity C. diphtheriae occurs in the respiratory tract, in wounds, or on the skin of infected persons or normal carriers. It is spread by droplets or skin contact. Portal of entry: respiratory tract or skin abrasions. Diphtheria bacilli colonize and grow on mucous membranes, and start to produce toxin, which is then absorbed into the mucous membranes, and even spread by the bloodstream. Local toxigenic effects: elicit inflammatory response and necrosis of the faucial mucosa cells-- formation of "pseudo- membrane“ (composed of bacteria, lymphocytes, plasma cells, fibrin, and dead cells), causing respiratory obstruction. Systemic toxigenic effects: necrosis in heart muscle, liver, kidneys and adrenals. Also produces neural damage. C. diphtheriae Clinical Diseases Respiratory diphtheria Incubation period: 2-4 days. Inflammation begins in the respiratory tract, causing sore throat, exudative pharyngitis that develops into pseudomembrane, and low grade fever. Prostration and dyspnea soon follow, which may lead to suffocation if not promptly relieved by intubation or tracheotomy. Myocarditis causing cardiac arrhythmias develops in many patients. Visual disturbance, difficulty in swallowing and paralysis of the arms and legs also occur but usually resolve spontaneously. Death may be due to asphyxia or heart failure. Cutaneous diphtheria: mild (papule ulcer with grayish membrane) with little toxigenic effects. Stimulates antitoxin production. C. diphtheriae Laboratory Diagnosis Specific treatment should be given before the lab reports if the clinical picture strongly suggests diphtheria. Specimens: swabs from the nose, throat or suspected lesions. Gram's stain: beaded rods in typical arrangement (unreliable). Culture: inoculate specimen onto a blood plate, and a selective medium like cysteine-tellurite blood plate. Identification: biochemical tests. Toxigenicity test: 1. Tissue culture neutralization assay. 2. in vitro test: immunodiffusion assay (Elek test ). 3. Detection of toxin gene by PCR. C. diphtheriae Treatment Treatment of diphtheria rests on prompt administration of antibiotics (penicillin or erythromycin) and diphtheria antitoxin. Maintenance of an open airway. Vaccination of recovered patients with toxoid is required because most patients fail to develop antitoxin antibodies. C. diphtheriae Prevention and Control Humans are the only
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