W1-4 Diseases Caused by Gram-Negative Bacteria Lecture PDF

Infectious - Diseases Caused by Gram-Negative Bacteria Objectives Discuss the different diseases caused by gram negative bacteria Discuss the pathogenesis of each disease Discuss the diagnostic modalities for each disease Discuss the treatment of diseases caused by gram negative bacteria ...

Infectious - Diseases Caused by Gram-Negative Bacteria Objectives Discuss the different diseases caused by gram negative bacteria Discuss the pathogenesis of each disease Discuss the diagnostic modalities for each disease Discuss the treatment of diseases caused by gram negative bacteria Gram Negative Bacteria Gram Negative Bacteria Gram-negative Bacteria Cocci Neisseria Characteristics nonmotile, catalase- and oxidase-positive, aerobic, Gram-negative cocci that are often arranged in pairs with flattened adjacent surfaces, giving the appearance of kidney or coffee beans Neisseria Clinical Manifestations N. meningitidis may colonize the mucous membranes of the upper respiratory tract, followed by formation of bactericidal and hemagglutinating antibodies (7-10d) In a few cases, disease results shortly after colonization, most frequently in the form of meningococcemia and meningitis. It may also invade serous membranes and joint tissues resulting to pleuritis, pericarditis and arthritis. Neisseria The virulence factor of N. meningitidis is a lipopolysaccharide– endotoxin complex, which activates the clotting cascade, depositing fibrin in small vessels, producing hemorrhage in the adrenals and other organs, altering peripheral vascular resistance, and leading to shock and death. N. gonorrhoeae (Type 1 and 2) adhere by means of pili → these may inhibit phagocytosis and stimulate strain-specific antibody formation. Neisseria Laboratory Diagnosis The pathogenic species are sensitive to drying and extremes of temperature, and material must be cultured promptly to enhance recovery. Direct inoculation of specimens ‘at the bedside’ followed by prompt incubation at 35°C in CO2 is optimal. All species of Neisseria are oxidase positive, and all species except N. elongata are catalase positive. Neisseria N. gonnorhoeae typically show gram negative diplococci. Confirmation of N. gonorrhoeae and identification of the other Neisseria spp. are based on growth and biochemical characteristics. Neisseria Antimicrobial Susceptibility Penicillin G is the drug of choice for meningococcal meningitis. Other agents that have good activity against N. meningitides include the extended-spectrum cephalosporins and chloramphenicol. Rifampin, minocycline, and the fluoroquinolones. Neisseria The current recommendations for treatment of N. gonorrhoeae include the extended-spectrum cephalosporins or the newer fluoroquinolones. Neisseria Prevention A polysaccharide vaccine against N. meningitidis serogroups A, C, Y, and W135. Rifampicin is the DOC for antibiotic prophylaxis. Moraxella catarrhalis an encapsulated organism, and extending from its outer membrane are pili that serve as adhesins Commonly causes bronchitis, otitis, sinusitis, and pneumonia. M. catarrhalis bacteria are oxidase- and catalase-positive, but can be differentiated from Neisseria sp. in their ability to grow readily on blood and chocolate agar, their lack of oxidative metabolism (sugars will be negative), and their production of DNase. Nearly all isolates of M. catarrhalis produce β-lactamaseNearly all isolates of M. catarrhalis produce β-lactamase. Gram-negative Bacteria Bacilli Enterobacteriaceae aerobic and facultatively anaerobic, non-spore-forming, non-motile or peritrichously flagellated, oxidase-negative, Gram-negative bacilli that produce acid fermentatively from glucose and reduce nitrates to nitrites. Enterobacteriaceae Clinical Manifestations and Pathogenesis Commonly causes abscesses, pneumonia, meningitis, septicemia, and urinary tract infections. Those commonly associated with human infection include E. coli, Klebsiella spp., Proteus spp., Enterobacter spp., Salmonella spp., Shigella spp., Serratia spp., Citrobacter spp., and Providencia spp. Gram-negative pneumonias are frequently caused by K. pneumoniae. Gram-negative bacteremias are frequently caused by E. coli, K. pneumoniae, and P. mirabilis. Enterobacteriaceae Endotoxins consist of lipid and polysaccharide moieties with small amounts of amino acids, and are often referred to as lipopolysaccharides. Lipopolysaccharides may elicit fever, chills, hypotension, granulocytosis, thrombocytopenia, DIC, and activation of both the classic and alternate complement pathways. Other pathogenetic factors of the Enterobacteriaceae include the K1 antigen, which is associated with a high percentage of strains of E. coli causing neonatal meningitis. Enterobacteriaceae K. pneumoniae capsule inhibits phagocytosis. Vi antigen of Salmonella serotype typhi, which may interfere with intracellular killing. Plasmid-mediated factors appear to play an important role in the invasive properties of Salmonella, Shigella, and enteroinvasive strains of E. coli. Heat-labile enterotoxins (LT) and heat-stable enterotoxins of E. coli are plasmid-mediated. Enterobacteriaceae Laboratory Diagnosis Eosin methylene blue (EMB) and MacConkey's agar can be used initially select for and differentiate lactose-fermenting from non-lactose-fermenting Gram- negative bacilli. XLD and HE agars are more selective differential media that are especially useful to select for Salmonella spp. and Shigella spp. Proteus spp. swarm on blood agar, Klebsiella spp. form mucoid colonies, Serratia marcescens may produce a red pigment, Salmonella spp. produce H2S, and E. coli is indole-positive. Enterobacteriaceae Enterobacteriaceae Antimicrobial Susceptibility E. coli and P. mirabilis are susceptible to ampicillin. Resistance to first-generation cephalosporins (cefazolin, cephalothin) is expected for Enterobacter spp., Serratia spp., Citrobacter spp., Proteus vulgaris, Providencia spp., Morganella spp., and Yersinia spp. Many of the members of enterobacteriaceae are susceptible to third- generation cephalosphorins, aminoglycosides and fluoroquinolones. Plesiomonas Plesiomonas shigelloides facultatively anaerobic, oxidase- and catalase-positive, glucose- fermenting, Gram-negative rod Plesiomonas Clinical Manifestations and Pathogenesis P. shigelloides is found in aquatic environments that are limited geographically by its minimum growth temperature of 8°C Causes gastroenteritis, especially following the ingestion of uncooked shellfish. Extraintestinal manifestations of infection include meningitis, septicemia, cellulitis, arthritis, and endophthalmitis. Plesiomonas Laboratory Diagnosis Can be isolated on a variety of nonselective and enteric-selective media, including HE agar It is indole-positive; reduces nitrates to nitrites; produces catalase; is methyl- red-positive; and ferments glucose, maltose, and trehalose. Antimicrobial Susceptibility P. shigelloides is susceptible to a variety of antimicrobial agents, including cephalosporins, trimethoprim–sulfamethoxazole, imipenem and the quinolones. Gram-negative Bacteria Nonfermentative Bacilli Pseudomonas strictly aerobic, catalase-positive, oxidase-positive, Gram-negative bacilli. Their metabolism is respiratory and never fermentative with oxygen as the terminal electron acceptor. Pseudomonas Clinical Manifestation and Pathogenesis Pulmonary infection occurs commonly in patients with cystic fibrosis. P. aeruginosa may produce serious infection in patients with burns, traumatic, and operative wounds; following urinary tract manipulation; in patients with diseases of the hematopoietic, reticuloendothelial, and lymphoid systems; and in those with impaired cellular or humoral defenses. Pseudomonas P. aeruginosa produces a slime polysaccharide, an endotoxin, and proteases that inactivate components of complement, thereby inhibiting to some degree opsonization and the inflammatory response and perhaps contributing to its invasiveness. Exotoxin A promotes cellular damage and tissue invasion and is toxic for macrophages. Pseudomonas Laboratory Diagnosis Has a musty grape-like (or corn tortilla) odor, the rough or ground- glass appearance of its colonies on sheep blood agar, and the presence of one or both of two pigments: a ‘blue-green’ fluorescent pigment and/or a metallic sheen due to pyoverdin pigment. Its identification can be made easily with a positive oxidase reaction, an alkaline slant/neutral butt reaction in TSIA, growth at 42°C, and the formation of sheen and/or pigment on the slants of TSIA and Pseudomonas P agar. Pseudomonas Antimicrobial Susceptibility Isolates are often susceptible to the aminoglycosides, the carboxy- and ureidopenicillins, ceftazidime or cefepime, carbapenems, and the quinolones. Acinetobacter short, rod-shaped to spherical, non-motile, oxidase-negative, strictly aerobic, and Gram-negative. commonly found in soil and water and uncommonly found on the skin and mucous membranes of healthy people. usually nonpathogenic, but they have been increasingly associated with nosocomial septicemia, pneumonia, bacteriuria, and wound infection. Acinetobacter Acinetobacter spp. can be distinguished readily from the pseudomonads on the basis of their lack of motility, inability to reduce nitrates, and negative oxidase reaction. Acinetobacter spp. are resistant to most available β-lactam and aminoglycoside antibiotics. Acinetobacter spp. may be susceptible to doxycycline, trimethoprim– sulfamethoxazole, quinolones, ureidopenicillins, imipenem, ampicillin–sulbactam, and ceftazidime. Burkholderia aerobic, non-spore-forming, Gram-negative rods and, except for Burkholderia mallei, are all motile because of having polar flagella. They are catalase-positive and most are oxidase-positive. These organisms are found in the environment in water, soil, and on plants. They have the potential to cause nosocomially acquired infections. Burkholderia Clinical Significance and Pathogenesis B. pseudomallei, which is acquired via inhalation or contact through cut or abraded skin, causes melioidosis. The infection can be asymptomatic, become chronic, or cause a fulminant sepsis. Melioidosis is most prevalent in south-east Asia and Australia but may also occur in other tropical and subtropical environments. Burkholderia B. cepacia, a nosocomial pathogen that is associated with contaminated equipment, medications, and disinfectants, can cause bacteremia, urinary tract infections, septic arthritis, and respiratory tract infections. Burkholderia species grow well on standard laboratory media including blood and chocolate agar. Burkholderia Antimicrobial Susceptibility B. cepacia is highly resistant to many antimicrobials but is usually susceptible to piperacillin, ceftazidime, chloramphenicol, and trimethoprim– sulfamethoxazole. Strains from cystic fibrosis patients who have been on repeated courses of antibiotics are likely to be resistant to these agents. Stenotrophomonas maltophilia A significant nosocomial pathogen. Risk factors for colonization or infection with this organism are mechanical ventilation, use of broad-spectrum antibiotics, catheterization, and neutropenia. S. maltophilia have negative oxidase reaction and positive DNase activity. Colonies grow on blood agar (lavender green colonies) and MacConkey's agar; the bacteria are nonmotile and nonfermentative. Stenotrophomonas maltophilia Antimicrobial Susceptibility S. maltophilia is inherently resistant to many antibiotics, in particular, the carbapenems. Trimethoprim–sulfamethoxazole is the antibiotic of choice. Vibrio facultatively anaerobic, oxidase-positive, short, curved, or straight Gram-negative bacilli that are usually motile by means of polar flagella, ferment carbohydrates, and reduce nitrates to nitrites. Vibrio Clinical Manifestations and Pathogenesis Vibrio vulnificus causes the most severe disease. Wound infections and septicemia with this organism are often fatal. Disease is usually associated with consumption of raw oysters or oyster- related injury. Decreased liver function results in increases in the available iron and appears to facilitate the growth of the organism. Vibrio Cholera toxin-producing Vibrio cholerae O1 is a well known cause of epidemic cholera. The cholera toxin mediates this effect by binding to and activating the adenylate cyclase of cells in the small intestine resulting in hypersecretion of electrolytes and water Vibrio mimicus and Vibrio parahaemolyticus primarily cause gastroenteritis. Vibrio Laboratory Diagnosis Growth of this group of organisms requires media containing NaCl except V. cholerae and V. mimicus. Selective media containing sucrose, such as thiosulfate citrate bile salts medium, are very useful for culturing stool specimens for Vibrio spp. Vibrio Antimicrobial Susceptibility Antimicrobial susceptibility testing can be performed using the disk diffusion method with Mueller–Hinton agar and the broth microdilution using cation- adjusted Mueller–Hinton broth and incubation at 35°C for 16-18 hours. CLSI has established interpretive standards for V. cholerae tested with ampicillin, tetracycline, doxycycline, trimethoprim–sulfamethoxazole, chloramphenicol, and sulfonamides. Aeromonas Facultatively anaerobic, oxidase- and catalase positive, rod-shaped, Gram-negative bacilli. They are usually motile by means of polar flagella, although some species may be nonmotile. They form acids from carbohydrates by respiratory and fermentative metabolism and reduce nitrates to nitrite. Aeromonas Clinical Manifestations and Pathogenesis mainly found in aquatic environments These organisms have been associated with both intestinal and extraintestinal disease. Its role in producing diarrheal disease is possibly related to the production of an enterotoxin by some strains. A hemolysin and a cytopathic factor have also been described. Aeromonas Laboratory Diagnosis The isolation of a fermenting, oxidase-positive, Gram-negative bacillus from an appropriate specimen should suggest the possibility of Aeromonas spp Antimicrobial Susceptibility Aeromonas spp. are susceptible to the quinolones, aminoglycosides, carbapenems, and trimethoprim–sulfamethoxazole but produce a β- lactamase that mediates resistance to the penicillins and first-generation cephalosporins Campylobacter small (0.5–8 μm long × 0.2-0.5 μm wide), motile, non-spore-forming, curved (comma-shaped) or S-shaped Gram-negative bacilli that grow optimally in an atmosphere containing 5-10% oxygen (microaerophilic). C. jejuni is the most common cause of bacterial enteritis in the United States. Campylobacter Campylobacter Clinical Manifestations and Pathogenesis C. jejuni infections generally occur in the summer and fall and are commonly the result of ingestion of improperly cooked foods, usually poultry. The diarrhea produced may be with or without blood or fecal leukocytes. Symptoms can last up to one week and are generally self-limited. Extraintestinal infections may also occur, including bacteremia, reactive arthritis, urinary tract infections, and meningitis. C. jejuni is the most recognized antecedent cause of Guillain–Barré syndrome. Campylobacter The pathogenesis of this organism is not completely understood; it appears to first colonize the intestinal mucous layer and then is able to translocate through the epithelial surface to the underlying tissue. The major habitat of C. fetus subsp. fetus is the intestine of sheep and cattle. Direct contact with an infected animal is a possible mode of transmission. Contaminated food or water may be a vehicle for infection, or infection may originate from an endogenous source. Campylobacter Laboratory Diagnosis A single stool specimen is generally adequate to detect enteric pathogens, including Campylobacter spp. Several media can be used for the selective isolation of Campylobacter spp., including charcoal–cefoperazone–deoxycholate agar, charcoal-based selective medium, semisolid blood-free motility medium, Skirrow's medium, and Campylobacter agar with 5% sheep blood and five antimicrobials (cephalothin, trimethoprim, vancomycin, polymyxin B, and amphotericin B). Campylobacter Microaerophilic (5% O2, 10% CO2, 85% N2) Campylobacter spp. produce gray, flat, irregular, spready colonies, which may become round, convex, and glistening as the moisture content in the media is reduced. A typical Gram stain appearance and a positive oxidase reaction from a colony growing on selective media at 42°C can be reported as Campylobacter spp. C. jejuni is able to hydrolyze hippurate and is susceptible to nalidixic acid and resistant to cephalothin. C. coli is hippuricase-negative. Strains of C. fetus subsp. fetus are resistant to nalidixic acid, fail to hydrolyze hippurate, and do not ordinarily grow at 42°C. Campylobacter Antimicrobial Susceptibility Most campylobacter are not susceptible to penicillins or cephalosporins. For intestinal infection, erythromycin is the drug of choice, with quinolones used as alternative therapy. Treatment is often not warranted. Helicobacter spiral-shaped or curved Gram-negative non-spore-forming bacilli, measuring 0.3-1.0 μm wide and 1.5-10 μm in length. They are motile by multiple bipolar or monopolar flagella, are microaerobic, and have a respiratory metabolism. Helicobacter Clinical Manifestations and Pathogenesis Helicobacter spp. are found in the gastrointestinal tracts of mammals and birds. Transmission from one host to another occurs through both oral–oral and fecal–oral routes. Infection with H. pylori may result in acute gastritis symptoms. Most infected patients develop chronic active gastritis, which may lead to nonulcer dyspepsia or duodenal ulcers. H. pylori has been associated with 90% of duodenal ulcers and nearly all gastric ulcers. Helicobacter Laboratory Diagnosis Urea breath test is a noninvasive test that detects urease activity of H. pylori by measuring 14C and 13C-labeled CO2 in the patient's expelled air after ingestion of labeled urea. Serologic assays are also widely used. For culture, tissue specimens should be maintained at 4°C and processed within 2 hours of collection. Processed specimens may be inoculated to one of several media, including brain–heart infusion (BHIA), Brucella, Columbia, or Skirrow's supplemented with horse blood, horse serum, or sheep blood. Helicobacter The addition of vancomycin, amphotericin, and cefsulodin are recommended as selective agents. Inoculated media should be incubated in a microaerobic atmosphere (5-10% CO2, 80-90% N2, and 5-10% O2) under high humidity at 35°C for 5-7 days. H. pylori generally produces small, gray, translucent colonies on these media, has the characteristic Gram-negative spiral appearance in stained smears, and is oxidase-, catalase-, and urease-positive. Helicobacter Antimicrobial Susceptibility Multidrug regimens are used to treat H. pylori infection. These usually include two antibiotics (metronidazole, clarithromycin, tetracycline, or amoxicillin) and an ‘antiacid’ or PPI. Haemophilus oxidase-positive, facultatively anaerobic, small, Gram-negative, pleomorphic rods or coccobacilli with a potential requirement for X (hemin) and/or V (NAD) factor. Haemophilus Clinical Manifestations and Pathogenesis Most Haemophilus spp. are normal inhabitants of the upper respiratory tract. Person-to-person spread occurs by respiratory droplets. Infections caused by Haemophilus spp. range from conjunctivitis and otitis media to meningitis and endocarditis. Those that are generally considered human pathogens are H. influenzae, Haemophilus parainfluenzae, Haemophilus ducreyi, and Haemophilus aphrophilus. Haemophilus The major virulence factor of H. influenzae is the polysaccharide capsule, of which there are six serotypes (a–f). Nontypeable strains of H. influenzae are most frequently associated with acute otitis media and acute exacerbations of chronic bronchitis. H. parainfluenzae is usually a commensal in the upper respiratory tract but may also cause serious illness, such as endocarditis. H. ducreyi is responsible for the sexually transmitted disease chancroid. Haemophilus Laboratory Diagnosis Isolation of Haemophilus spp. usually requires the presence of X and/or V factor in the culture medium. Haemophilus H. ducreyi Haemophilus Antimicrobial Susceptibility CLSI recommends testing H. influenzae isolated from blood or CSF against ampicillin, chloramphenicol, a third-generation cephalosporin, and meropenem The recommended treatment for H. ducreyi infection is erythromycin; alternative agents include azithromycin, ciprofloxacin, ceftriaxone, amoxicillin–clavulanate, and trimethoprim–sulfamethoxazole. Gram-negative Bacteria The HACEK Bacteria The HACEK Bacteria five small Gram-negative coccobacilli that are part of the normal oral flora and are occasionally associated with bacterial endocarditis and rarely other infections. The word HACEK stands for: H aemophilus sp. (influenzae, parainfluenzae, and aphrophilus most commonly), Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella sp. Actinobacillus A. actinomycetemcomitans is a Gram-negative, non-spore-forming coccobacillus or short rod. It grows both aerobically and anaerobically. found in the mucous membranes of the respiratory and genitourinary tract of humans and animals. They generally cause disease only in immunocompromised individuals or when they are accidentally introduced into healthy surrounding tissue, for example, by trauma. Actinobacillus it has most frequently been reported as a cause of subacute bacterial endocarditis, periodontitis, and brain abscess. Two virulence factors are known: a leukotoxin and a collagenase. A. actinomycetemcomitans grows on blood and chocolate agar. After 24-72 hours, colonies are 1–3 mm in diameter with a central wrinkling. The organism is catalase positive, oxidase negative or weakly positive, and urease negative. Actinobacillus This organism is resistant to penicillin but is usually susceptible to many other antibiotics including the cephalosporins, β-lactam–β- lactamase inhibitor combinations, fluoroquinolones, and tetracycline. Cardiobacterium hominis Gram-negative, non-spore-forming bacillus that is part of the normal oral flora. Facultative anaerobe that does not require CO2, although growth is enhanced in microaerophilic conditions. Growth occurs on blood and chocolate agar but not on MacConkey's agar and is better at longer than 48 hours. Cardiobacterium hominis Cardiobacterium hominis can cause subacute bacterial endocarditis and may also be responsible for cases of periodontitis. Colonies at 48 hours incubation are small and may have a yellow- white pigment. The organism is generally oxidase- and indole-positive but negative for catalase, urease, esculin, and nitrate reduction. Acid may be produced from glucose, maltose and sucrose. Cardiobacterium hominis Isolates are usually susceptible to penicillins and cephalosporins, aminoglycosides, and tetracyclines. Resistance to clindamycin is common. No β-lactamases have been reported as yet. Eikenella E. corrodens organisms are oxidase-positive, catalase- negative, nonfermentative, Gram-negative bacilli, colonies of which may corrode or pit agar. Growth is enhanced by 5-10% CO2 and usually requires the presence of X factor in the medium. E. corrodens resides predominantly in the oral cavity and is isolated frequently from the upper respiratory tract. It is responsible for subacute bacterial endocarditis. It has been recovered from abscesses, cellulitis, and wound infections, often following human bites. Eikenella Growth is observed on blood or chocolate agar but not MacConkey agar. The most striking features of E. corrodens in culture are the distinctive odor of bleach and characteristic pitting of the agar. The colonies appear slowly (2-4 days) and are generally small (0.5-1.0 mm in diameter). E. corrodens is susceptible to the penicillins, quinolones, and tetracycline and resistant to clindamycin and metronidazole. Kingella 3 species: K. kingae (the HACEK species), Kingella oralis, and Kingella denitrificans. They are Gram-negative rods to coccobacilli, requiring increased CO2 for optimum growth. Colonies will grow on blood (β-hemolytic) and chocolate, but not MacConkey agar after 2 days. K. kingae is the most pathogenic of the three species causing a indolent, slowly progressive endocarditis. It is associated with septic arthritis/osteomyelitis, usually in children, and septicemia. Kingella K. kingae is oxidase-positive and produces acid from glucose, although in delayed fashion. Indole and catalase are negative. K. kingae is susceptible to penicillin and most other antibiotics to which other members of the HACEK group are susceptible. Gram-negative Bacteria Miscellaneous Legionella non-spore-forming, faintly staining, thin, Gram-negative bacilli. The majority of clinical cases have been due to Legionella pneumophila, serogroup 1. Legionella Legionella spp. are found in the environment in association with water. Transmission to humans occurs through exposure to contaminated water. Infections can be subclinical, pulmonary, or extrapulmonary. Infection is usually manifested as an acute, fibrinopurulent pneumonia with lobular distribution. Histologically, there is an alveolar infiltrate of neutrophils and macrophages, accompanied by fibrin and red blood cell extravasation. Legionella spp. may be found within alveolar macrophages. Legionella may be isolated on BCYE agar supplemented with growth factors, including l-cystine, ferric salt, and α-ketoglutarate. Colonies will often appear iridescent and have a sticky consistency. These organisms may be weakly oxidase- and catalase-positive, will be gelatinase-positive, and often motile. Legionella Susceptibility testing should not be performed. Therapy generally consists of erythromycin and rifampin. Other agents that have been used include trimethoprim–sulfamethoxazole, quinolones, clarithromycin, and azithromycin. Bordetella strictly aerobic, nonfermentative, minute coccobacilli requiring nicotinic acid, cysteine, and usually methionine but not X or V factor for growth. Bordetella spp. are found in the respiratory tracts of warm-blooded animals. B. pertussis, the etiologic agent of whooping cough, only causes disease in humans. Bordetella Adenylate cyclase toxin inhibits immune effector and other cell functions by creating a high intracellular level of cyclic adenosine 3′,5′-phosphate. Tracheal cytotoxin causes cell ciliostasis and cell death. Filamentous hemagglutinin, pertactin, and fimbras are involved in adhesion. B. pertussis also produces pertussis toxin, which inhibits intracellular signal transduction factors by transferring adenosine diphosphate ribose to G proteins of cells. Bordetella most commonly recommended specimen is the nasopharyngeal swab. Direct examination of smears stained with fluorescein-conjugated B. pertussis monoclonal or polyclonal antiserum may provide a rapid diagnosis. Cultures should be incubated in a humid environment at 35°C without addition of CO2. B. pertussis grows slowly and should be held for 7-12 days before being discarded as negative. Colonies are small, smooth, round, and shiny and may have the appearance of a drop of mercury. Bordetella Positive catalase and oxidase reactions and negative urease can be used for presumptive identification of an organism as B. pertussis. Susceptibility testing is not indicated for B. pertussis. Erythromycin is the drug of choice for treatment and prophylaxis; trimethoprim–sulfamethoxazole is an acceptable alternative. References Jawetz, Melnick, & Adelberg's Medical Microbiology. 23rd ed. New York, N.Y.: Lange Medical Books/McGraw-Hill, Medical Pub. Division, 2004. Tille, Patricia M., author. Bailey & Scott's Diagnostic Microbiology. St. Louis, Missouri :Elsevier, 2014.