-Positive Cocci (Chapter 15) >
| Staphylococcus aureus Diseases Abscesses of many organs, endocarditis, gastroenteritis (food poisoning), toxic shock syndrome, hospital-acquired pneumonia, surgical wound infections, and sepsis. It is one of the most common causes of human infections. Characteristics Gram-positive cocci in clusters. Coagulase-positive. Catalase-positive. Most isolates produce [ندعوك للتسجيل في المنتدى أو التعريف بنفسك لمعاينة هذه الصورة]-lactamase. Habitat and Transmission Main habitat is human nose; also found on human skin. Transmission is via the hands. Pathogenesis Abscess containing pus is the most common lesion. Three exotoxins are also made. Toxic shock syndrome toxin is a superantigen and causes toxic shock syndrome by stimulating many helper T cells to release large amounts of lymphokines, especially IL-2. Enterotoxin, which causes food poisoning, is also a superantigen. Food poisoning has a short incubation period because it is preformed in food. Scalded skin syndrome toxin is a protease that cleaves desmoglein in tight junctions in the skin. Protein A is an important virulence factor because it binds to the heavy chain of IgG and prevents the activation of complement. Predisposing factors to infection include breaks in the skin, foreign bodies such as sutures, neutrophil levels below 500/[ندعوك للتسجيل في المنتدى أو التعريف بنفسك لمعاينة هذه الصورة]L, intravenous drug use (predisposes to right-sided endocarditis), and tampon use (predisposes to toxic shock syndrome). Laboratory Diagnosis Gram-stained smear and culture. Yellow or gold colonies on blood agar. Staphylococcus aureus is coagulase-positive; Staphylococcus epidermidis is coagulase-negative. Serologic tests not useful. Treatment Penicillin G for sensitive isolates; [ندعوك للتسجيل في المنتدى أو التعريف بنفسك لمعاينة هذه الصورة]-lactamase-resistant penicillins such as nafcillin for resistant isolates; vancomycin for isolates resistant to nafcillin. About 85% are resistant to penicillin G. Plasmid-encoded [ندعوك للتسجيل في المنتدى أو التعريف بنفسك لمعاينة هذه الصورة]-lactamase mediates most resistance. Resistance to nafcillin is caused by changes in binding proteins. Some isolates are tolerant to penicillin. Rare vancomycin-resistant strains have emerged. Prevention Cefazolin is used to prevent surgical wound infections. No vaccine is available. Hand washing reduces spread. |
| Staphylococcus epidermidis Diseases Endocarditis on prosthetic heart valves, prosthetic hip infection, intravascular catheter infection, cerebrospinal fluid shunt infection, neonatal sepsis. Characteristics Gram-positive cocci in clusters. Coagulase-negative. Catalase-positive. Habitat and Transmission Normal flora of the human skin and mucous membranes. It is probably the patient's own strains that cause infection, but transmission from person to person via hands may occur. Pathogenesis Glycocalyx-producing strains adhere well to foreign bodies such as prosthetic implants and catheters. It is a low-virulence organism that causes disease primarily in immunocompromised patients and in those with implants. It is a major cause of hospital-acquired infections. Unlike S. aureus, no exotoxins have been identified. Laboratory Diagnosis Gram-stained smear and culture. Whitish, non-hemolytic colonies on blood agar. It is coagulase-negative. S. epidermidis is sensitive to novobiocin, whereas the other coagulase-negative staphylococcus, S. saprophyticus, is resistant. Serologic tests are not useful. Treatment Vancomycin plus either rifampin or an aminoglycoside. It produces [ندعوك للتسجيل في المنتدى أو التعريف بنفسك لمعاينة هذه الصورة]-lactamases and is resistant to many antibiotics. Prevention There is no drug or vaccine. |
| Staphylococcus saprophyticus Gram-positive cocci in clusters. Coagulase-negative. Resistant to novobiocin in contrast to S. epidermidis, which is sensitive. Causes community-acquired urinary tract infections in young women (but Escherichia coli is a much more common cause). |
| Streptococcus pyogenes (Group A Streptococcus) Diseases Suppurative (pus-producing) diseases, e.g., pharyngitis and cellulitis; nonsuppurative (immunologic) diseases, e.g., rheumatic fever and acute glomerulonephritis. Characteristics Gram-positive cocci in chains. Beta-hemolytic. Catalase-negative. Bacitracin-sensitive. Beta-hemolytic streptococci are subdivided into group A, B, etc., by differences in the antigenicity of their cell wall carbohydrate. Habitat and Transmission Habitat is the human throat and skin. Transmission is via respiratory droplets. Pathogenesis For suppurative infections, hyaluronidase ("spreading factor") mediates subcutaneous spread seen in cellulitis; erythrogenic toxin (a superantigen) causes the rash of scarlet fever; M protein impedes phagocytosis. For nonsuppurative (immunologic) diseases, rheumatic fever is caused by immunologic cross-reaction between bacterial antigen and human heart and joint tissue (i.e., antibody against streptococcal M protein reacts with myosin in cardiac muscle), and acute glomerulonephritis is caused by immune complexes formed between streptococcal antigens and antibody to those antigens. The immune complexes are trapped by glomeruli, complement is activated, neutrophils are attracted to the site by C5a, and proteases produced by neutrophils damage glomeruli. Laboratory Diagnosis The diagnosis of suppurative infections, e.g., cellulitis, differs from immunologic diseases, e.g., rheumatic fever. For suppurative infections, use Gram-stained smear and culture. Beta-hemolytic colonies on blood agar. (Hemolysis due to streptolysins O and S.) If isolate is sensitive to bacitracin, it is identified as Streptococcus pyogenes. Rapid ELISA tests for group A streptococcal antigens in throat swabs are available. Assay for antibody in patient's serum is not done for suppurative infections. If rheumatic fever is suspected, patient's antistreptolysin O (ASO) antibody titer is tested to determine whether previous exposure to S. pyogenes has occurred. If acute glomerulonephritis is suspected, antibody to streptococcal DNase B is used as evidence of a previous skin infection by S. pyogenes. Treatment Penicillin G (no significant resistance). Prevention Penicillin is used in patients with rheumatic fever to prevent recurrent S. pyogenes pharyngitis. This prevents additional damage to heart valves. There is no vaccine. |
| Streptococcus agalactiae (Group B Streptococcus) Diseases Neonatal meningitis and sepsis. Characteristics Gram-positive cocci in chains. Beta-hemolytic. Catalase-negative. Bacitracin-resistant. Beta-hemolytic streptococci are subdivided into group A, B, etc., by differences in the antigenicity of their cell wall carbohydrate. Habitat and Transmission Main habitat is the human vagina. Transmission occurs during birth. Pathogenesis Pyogenic organism. No exotoxins identified. Predisposing factors to neonatal infection include rupture of membranes more than 18 hours before delivery, labor prior to 37 weeks (infant is premature), absence of maternal antibody, and heavy colonization of the genital tract by the organism. Laboratory Diagnosis Gram-stained smear and culture. Beta-hemolytic (narrow zone) colonies on blood agar that are resistant to bacitracin. Organisms hydrolyze hippurate and are CAMP test–positive. Treatment Penicillin G. Prevention No vaccine. Ampicillin should be given to mothers if prolonged rupture of membranes occurs, if mother has a fever, or if the neonate is premature. |
| Enterococcus faecalis Diseases Urinary tract and biliary tract infections are most frequent. Endocarditis rare but life-threatening. Characteristics Gram-positive cocci in chains. Catalase-negative. Habitat and Transmission Habitat is the human colon; urethra and female genital tract can be colonized. May enter bloodstream during gastrointestinal (GI) or genitourinary tract procedures. May infect other sites, e.g., endocarditis. Pathogenesis No exotoxins or virulence factors identified. Laboratory Diagnosis Gram-stained smear and culture. Alpha-, beta-, or nonhemolytic colonies on blood agar. Grows in 6.5% NaCl and hydrolyzes esculin in the presence of 40% bile. Serologic tests not useful. Treatment Penicillin or vancomycin plus an aminoglycoside such as gentamicin is bactericidal. Organism is resistant to either drug given individually, but given together they have a synergistic effect. Aminoglycoside alone is ineffective because it cannot penetrate. Penicillin or vancomycin weakens the cell wall, allowing the aminoglycoside to penetrate. Vancomycin-resistant enterococci (VRE) are important causes of nosocomial (hospital-acquired) infections. Linezolid can be used to treat VRE. Prevention Penicillin and gentamicin should be given to patients with damaged heart valves prior to intestinal or urinary tract procedures. No vaccine is available. |
| Streptococcus pneumoniae (Pneumococcus) Diseases The most common diseases are pneumonia and meningitis in adults and otitis media and sinusitis in children. Characteristics Gram-positive "lancet-shaped" cocci in pairs (diplococci) or short chains. Alpha-hemolytic. Catalase-negative. Sensitive to bile and optochin in contrast to viridans streptococci, which are resistant. Prominent polysaccharide capsule. 85 serotypes based on antigenicity of polysaccharide capsule. One of the three classical encapsulated pyogenic bacteria (Neisseria meningitidis and Haemophilus influenzae are the other two). Habitat and Transmission Habitat is the human upper respiratory tract. Transmission is via respiratory droplets. Pathogenesis Induces inflammatory response. No known exotoxins. Polysaccharide capsule retards phagocytosis. Antipolysaccharide antibody opsonizes the organism and provides type-specific immunity. IgA protease degrades secretory IgA on respiratory mucosa, allowing colonization. Viral respiratory infection predisposes to pneumococcal pneumonia by damaging mucociliary elevator; splenectomy predisposes to sepsis. Skull fracture with spinal fluid leakage from nose predisposes to meningitis. Laboratory Diagnosis Gram-stained smear and culture. Alpha-hemolytic colonies on blood agar. Growth inhibited by bile and optochin. Quellung reaction occurs (swelling of capsule with type-specific antiserum). Serologic tests for antibody not useful. Latex agglutination test for capsular antigen in spinal fluid can be diagnostic. Treatment Penicillin G. Low-level and high-level resistance is caused by alterations in penicillin-binding proteins. No [ندعوك للتسجيل في المنتدى أو التعريف بنفسك لمعاينة هذه الصورة]-lactamase is made. Prevention Two vaccines are available. The one used in adults contains capsular polysaccharide of the 23 serotypes that cause bacteremia most frequently. The other, which is used primarily in children under the age of 2 years, contains capsular polysaccharide of 7 serotypes coupled to carrier protein (diphtheria toxoid). Oral penicillin is used in immunocompromised children. |
| Viridans Group Streptococci (e.g., S. sanguis, S. mutans) Diseases Endocarditis is the most important. Also brain abscess, especially in mixed infections with mouth anaerobes. S. mutans implicated in dental caries. Characteristics Gram-positive cocci in chains. Alpha-hemolytic. Catalase-negative. Resistant to bile and optochin in contrast to pneumococci, which are sensitive. Habitat and Transmission Habitat is the human oropharynx. Organism enters bloodstream during dental procedures. Pathogenesis Bacteremia from dental procedures spreads organism to damaged heart valves. Organism is protected from host defenses within vegetations. No known toxins. Glycocalyx composed of polysaccharide enhances adhesion to heart valves. Laboratory Diagnosis Gram-stained smear and culture. Alpha-hemolytic colonies on blood agar. Growth not inhibited by bile or optochin, in contrast to pneumococci. Viridans streptococci are classified into species by using various biochemical tests. Serologic tests not useful. Treatment Penicillin G with or without an aminoglycoside. Prevention Penicillin to prevent endocarditis in patients with damaged or prosthetic heart valves who undergo dental procedures. |
| Neisseria meningitidis (Meningococcus) Diseases Meningitis and meningococcemia. Characteristics Gram-negative "kidney-bean" diplococci. Oxidase-positive. Large polysaccharide capsule. One of the three classic encapsulated pyogenic bacteria (Streptococcus pneumoniae and Haemophilus influenzae are the other two). Habitat and Transmission Habitat is the human upper respiratory tract; transmission is via respiratory droplets. Pathogenesis After colonizing the upper respiratory tract, the organism reaches the meninges via the bloodstream. Endotoxin in cell wall causes symptoms of septic shock seen in meningococcemia. No known exotoxins; IgA protease produced. Capsule is antiphagocytic. Deficiency in late complement components predisposes to recurrent meningococcal infections. Laboratory Diagnosis Gram-stained smear and culture. Oxidase-positive colonies on chocolate agar. Ferments maltose in contrast to gonococci, which do not. Serologic tests not useful. Treatment Penicillin G (no significant resistance). Prevention Vaccine contains capsular polysaccharide of strains A, C, Y, and W-135. One form of the vaccine contains the polysaccharides coupled to a carrier protein (diphtheria toxoid) and one contains only the polysaccharides. Rifampin or ciprofloxacin given to close contacts to decrease oropharyngeal carriage. |
| Neisseria gonorrhoeae (Gonococcus) Disease Gonorrhea. Also neonatal conjunctivitis and pelvic inflammatory disease. Characteristics Gram-negative "kidney-bean" diplococci. Oxidase-positive. Insignificant capsule. Habitat and Transmission Habitat is the human genital tract. Transmission in adults is by sexual contact. Transmission to neonates is during birth. Pathogenesis Organism invades mucous membranes and causes inflammation. Endotoxin present but weaker than that of meningococcus, so less severe disease when bacteremia occurs. No exotoxins identified. IgA protease and pili are virulence factors. Laboratory Diagnosis Gram-stained smear and culture. Organism visible intracellularly within neutrophils in urethral exudate. Oxidase-positive colonies on Thayer-Martin medium. Gonococci do not ferment maltose, whereas meningococci do. Serologic tests not useful. Treatment Ceftriaxone for uncomplicated cases. Tetracycline added for urethritis caused by Chlamydia trachomatis. High-level resistance to penicillin is caused by plasmid-encoded penicillinase. Low-level resistance to penicillin is caused by reduced permeability and altered binding proteins. Prevention No drug or vaccine. Condoms offer protection. Trace contacts and treat to interrupt transmission. Treat eyes of newborns with erythromycin ointment or silver nitrate to prevent conjunctivitis. |
| Bacillus anthracis Disease Anthrax. Characteristics Aerobic, gram-positive, spore-forming rods. Capsule composed of poly-D-glutamate. B. anthracis is the only medically important organism that has a capsule composed of amino acids rather than polysaccharides. Habitat and Transmission Habitat is soil. Transmission is by contact with infected animals or inhalation of spores from animal hair and wool. Pathogenesis Anthrax toxin consists of three proteins: edema factor, which is an adenylate cyclase; lethal factor, which kills cells by inhibiting a signal transduction protein involved in cell division; and protective antigen, which mediates the entry of the other two components into the cell. The capsule is antiphagocytic. Laboratory Diagnosis Gram-stained smear plus aerobic culture on blood agar. B. anthracis is nonmotile, in contrast to other Bacillus species. Rise in antibody titer in indirect hemagglutination test is diagnostic. Treatment Penicillin G (no significant resistance). Prevention Vaccine consisting of protective antigen is given to individuals in high-risk occupations. |
| Bacillus cereus Disease Food poisoning. Characteristics Aerobic, gram-positive, spore-forming rod. Habitat and Transmission Habitat is grains, such as rice. Spores survive boiling during preparation of rice, then germinate when rice held at warm temperature. Pathogenesis Two enterotoxins are produced: one acts like cholera toxin, i.e., cyclic AMP is increased within enterocytes; the other acts like staphylococcal enterotoxin, i.e., it is a superantigen. Laboratory Diagnosis Not done. Treatment Symptomatic only. Prevention No vaccine. |
| Clostridium tetani Disease Tetanus. Characteristics Anaerobic, gram-positive, spore-forming rods. Spore is at one end ("terminal spore") so organism looks like a "tennis racket." Habitat and Transmission Habitat is the soil. Organism enters through traumatic breaks in the skin. Pathogenesis Spores germinate under anaerobic conditions in the wound. Organism produces exotoxin, which blocks release of inhibitory neurotransmitters (glycine and GABA) from spinal neurons. Excitatory neurons are unopposed, and extreme muscle spasm (tetanus, spastic paralysis) results. "Lockjaw" and "risus sardonicus" are two examples of the muscle spasms. Tetanus toxin (tetanospasmin) is a protease that cleaves proteins involved in the release of neurotransmitters. Laboratory Diagnosis Primarily a clinical diagnosis. Organism is rarely isolated. Serologic tests not useful. Treatment Hyperimmune human globulin to neutralize toxin. Also penicillin G and spasmolytic drugs (e.g., Valium). No significant resistance to penicillin. Prevention Toxoid vaccine (toxoid is formaldehyde-treated toxin). Usually given to children in combination with diphtheria toxoid and pertussis vaccine (DTaP). If patient is injured and has not been immunized, give hyperimmune globulin plus toxoid (passive-active immunization). Debride wound. Give tetanus toxoid booster every 10 years. |
| Clostridium botulinum Disease Botulism. Characteristics Anaerobic, gram-positive, spore-forming rods. Habitat and Transmission Habitat is the soil. Organism and botulinum toxin transmitted in improperly preserved food. Pathogenesis Botulinum toxin is a protease that cleaves proteins involved in the release of acetylcholine at the myoneural junction, causing flaccid paralysis. Failure to sterilize food during preservation allows spores to survive. Spores germinate in anaerobic environment and produce toxin. The toxin is heat-labile; therefore, foods eaten without proper cooking are usually implicated. Laboratory Diagnosis Presence of toxin in patient's serum or stool or in food. Detection of toxin involves either antitoxin in serologic tests or production of the disease in mice. Serologic tests for antibody in the patient are not useful. Treatment Antitoxin to types A, B, and E made in horses. Respiratory support may be required. Prevention Observing proper food preservation techniques, cooking all home-canned food, and discarding bulging cans. |
| Clostridium perfringens Diseases Gas gangrene (myonecrosis) and food poisoning. Characteristics Anaerobic, gram-positive, spore-forming rods. Habitat and Transmission Habitat is soil and human colon. Myonecrosis results from contamination of wound with soil or feces. Food poisoning is transmitted by ingestion of contaminated food. Pathogenesis Gas gangrene in wounds is caused by germination of spores under anaerobic conditions and the production of several cytotoxic factors, especially alpha toxin, a lecithinase that cleaves cell membranes. Gas in tissue (CO2 and H2) is produced by organism's anaerobic metabolism. Food poisoning is caused by production of enterotoxin within the gut. Enterotoxin acts as a superantigen, similar to that of S. aureus. Laboratory Diagnosis Gram-stained smear plus anaerobic culture. Spores not usually seen in clinical specimens; the organism is growing, and nutrients are not restricted. Production of lecithinase is detected on egg yolk agar and identified by enzyme inhibition with specific antiserum. Serologic tests not useful. Treatment Penicillin G plus debridement of the wound in gas gangrene (no significant resistance to penicillin). Only symptomatic treatment needed in food poisoning. Prevention Extensive debridement of the wound plus administration of penicillin decreases probability of gas gangrene. There is no vaccine. |
| Clostridium difficile Disease Pseudomembranous colitis. Characteristics Anaerobic, gram-positive, spore-forming rods. Habitat and Transmission Habitat is the human colon. Transmission is fecal–oral. Pathogenesis Antibiotics suppress normal flora of colon, allowing C. difficile to overgrow and produce large amounts of exotoxins. Exotoxins A and B inhibit GTPases, causing inhibition of signal transduction and depolymerization of actin filaments. This leads to apoptosis and death of enterocytes. The pseudomembranes seen in the colon are the visual result of the death of enterocytes. Laboratory Diagnosis Exotoxin in stool detected by cytopathic effect on cultured cells. Identified by neutralization of cytopathic effect with antibody. Exotoxin in the stool can also be detected by using an ELISA test. Treatment Metronidazole. Vancomycin, although effective, should not be used because it may select for vancomycin-resistant enterococci. Prevention No vaccine or drug is available. |
| Corynebacterium diphtheriae Disease Diphtheria. Characteristics Club-shaped gram-positive rods arranged in V or L shape. Granules stain metachromatically. Aerobic, non-spore-forming organism. Habitat and Transmission Habitat is the human throat. Transmission is via respiratory droplets. Pathogenesis Organism secretes an exotoxin that inhibits protein synthesis by adding ADP-ribose to elongation factor-2 (EF-2). Toxin has two components: subunit A, which has the ADP-ribosylating activity, and subunit B, which binds the toxin to cell surface receptors. Pseudomembrane in throat caused by death of mucosal epithelial cells. Laboratory Diagnosis Gram-stained smear and culture. Black colonies on tellurite plate. Document toxin production with precipitin test or by disease produced in laboratory animals. Serologic tests not useful. Treatment Antitoxin made in horses neutralizes the toxin. Penicillin G kills the organism. No significant resistance to penicillin. Prevention Toxoid vaccine (toxoid is formaldehyde-treated toxin), usually given to children in combination with tetanus toxoid and pertussis vaccine (DTaP). |
| Listeria monocytogenes Diseases Meningitis and sepsis in newborns and immunocompromised adults. Gastroenteritis. Characteristics Small gram-positive rods. Aerobic, non-spore-forming organism. Habitat and Transmission Organism colonizes the GI and female genital tracts; in nature it is widespread in animals, plants, and soil. Transmission is across the placenta or by contact during delivery. Outbreaks of sepsis in neonates and gastroenteritis in the general population are related to ingestion of unpasteurized milk products, e.g., cheese. Pathogenesis Listeriolysin is an exotoxin that degrades cell membranes. Reduced cell-mediated immunity and immunologic immaturity as in neonates predispose to disease. Intracellular pathogen that moves from cell-to-cell via "actin rockets." Laboratory Diagnosis Gram-stained smear and culture. Small, beta-hemolytic colonies on blood agar. Tumbling motility. Serologic tests not useful. Treatment Ampicillin with or without gentamicin. Prevention Pregnant women and immunocompromised patients should not ingest unpasteurized milk products or raw vegetables. Trimethoprim-sulfamethoxazole given to immunocompromised patients to prevent Pneumocystis pneumonia also can prevent listeriosis. No vaccine is available. |
| Escherichia coli Diseases Urinary tract infection (UTI), sepsis, neonatal meningitis, and "traveler's diarrhea" are the most common. Characteristics Facultative gram-negative rods; ferment lactose. Habitat and Transmission Habitat is the human colon; it colonizes the vagina and urethra. From the urethra, it ascends and causes UTI. Acquired during birth in neonatal meningitis and by the fecal–oral route in diarrhea. Pathogenesis Endotoxin in cell wall causes septic shock. Two enterotoxins are produced. The heat-labile toxin (LT) stimulates adenylate cyclase by ADP-ribosylation. Increased cyclic AMP causes outflow of chloride ions and water, resulting in diarrhea. The heat-stable toxin (ST) causes diarrhea, perhaps by stimulating guanylate cyclase. Virulence factors include pili for attachment to mucosal surfaces and a capsule that impedes phagocytosis. Verotoxin (Shiga-like toxin) is an enterotoxin produced by E. coli strains with the O157:H7 serotype. It causes bloody diarrhea and hemolytic-uremic syndrome associated with eating undercooked meat. Verotoxin inhibits protein synthesis by removing adenine from the 28S rRNA of human ribosomes. Predisposing factors to UTI in women include the proximity of the anus to the vagina and urethra, as well as a short urethra. This leads to colonization of the urethra and vagina by the fecal flora. Abnormalities, e.g., strictures, valves, and stones, predispose as well. Indwelling urinary catheters and intravenous lines predispose to UTI and sepsis, respectively. Colonization of the vagina leads to neonatal meningitis acquired during birth. Laboratory Diagnosis Gram-stained smear and culture. Lactose-fermenting colonies on EMB or MacConkey's agar. Green sheen on EMB agar. TSI agar shows acid slant and acid butt with gas but no H2S. Differentiate from other lactose-positive organisms by biochemical reactions. For epidemiologic studies, type organism by O and H antigens by using known antisera. Serologic tests for antibodies in patient's serum not useful. Treatment Ampicillin or sulfonamides for urinary tract infections. Third-generation cephalosporins for meningitis and sepsis. Rehydration is effective in traveler's diarrhea; trimethoprim-sulfamethoxazole may shorten duration of symptoms. Antibiotic resistance mediated by plasmid-encoded enzymes, e.g., [ندعوك للتسجيل في المنتدى أو التعريف بنفسك لمعاينة هذه الصورة]-lactamase and aminoglycoside-modifying enzymes. Prevention Prevention of UTI involves limiting the frequency and duration of urinary catheterization. Prevention of sepsis involves promptly removing or switching sites of intravenous lines. Traveler's diarrhea is prevented by eating only cooked food and drinking boiled water in certain countries. Prophylactic doxycycline or Pepto-Bismol may prevent traveler's diarrhea. There is no vaccine that prevents any of the diseases caused by E. coli. |
| Salmonella typhi Disease Typhoid fever. Characteristics Facultative gram-negative rods. Non-lactose-fermenting. Produces H2S. Habitat and Transmission Habitat is the human colon only, in contrast to other salmonellae, which are found in the colon of animals as well. Transmission is by the fecal–oral route. Pathogenesis Infects the cells of the reticuloendothelial system, especially in the liver and spleen. Endotoxin in cell wall causes fever. Capsule (Vi antigen) is a virulence factor. No exotoxins known. Decreased stomach acid resulting from ingestion of antacids or gastrectomy predisposes to Salmonella infections. Chronic carrier state established in gallbladder. Organism excreted in bile results in fecal–oral spread to others. Laboratory Diagnosis Gram-stained smear and culture. Non-lactose-fermenting colonies on EMB or MacConkey's agar. TSI agar shows alkaline slant and acid butt, with no gas and a small amount of H2S. Biochemical and serologic reactions used to identify species. Identity can be determined by using known antisera against O, H, and Vi antigens in agglutination test. Widal test detects agglutinating antibodies to O and H antigens in patient's serum, but its use is limited. Treatment Most effective drug is ceftriaxone. Ampicillin and trimethoprim-sulfamethoxazole can be used in patients who are not severely ill. Resistance to chloramphenicol and ampicillin is mediated by plasmid-encoded acetylating enzymes and [ندعوك للتسجيل في المنتدى أو التعريف بنفسك لمعاينة هذه الصورة]-lactamase, respectively. Prevention Public health measures, e.g., sewage disposal, chlorination of the water supply, stool cultures for food handlers, and hand washing prior to food handling. Two vaccines are in common use; one vaccine contains purified Vi polysaccharide capsule as the immunogen and the other contains live, attenuated S. typhi as the immunogen. |
| Salmonella enteritidis (Also Known as Salmonella enterica) Diseases Enterocolitis. Sepsis with metastatic abscesses occasionally. Characteristics Facultative gram-negative rods. Non-lactose-fermenting. Produces H2S. Motile, in contrast to Shigella. More than 1500 serotypes. Habitat and Transmission Habitat is the enteric tract of humans and animals, e.g., chickens and domestic livestock. Transmission is by the fecal–oral route. Pathogenesis Invades the mucosa of the small and large intestines. Can enter blood, causing sepsis. Infectious dose is at least 105 organisms, much greater than the infectious dose of Shigella. Infectious dose is high because organism is inactivated by stomach acid. Endotoxin in cell wall; no exotoxin. Predisposing factors include lowered stomach acidity from either antacids or gastrectomy. Sickle cell anemia predisposes to Salmonella osteomyelitis. Laboratory Diagnosis Gram-stained smear and culture. Non-lactose-fermenting colonies on EMB or MacConkey's agar. TSI agar shows alkaline slant and acid butt, with gas and H2S. Biochemical and serologic reactions used to identify species. Can identify the organism by using known antisera in agglutination assay. Widal test detects antibodies in patient's serum to the O and H antigens of the organism but is not widely used. Treatment Antibiotics usually not recommended for uncomplicated enterocolitis. Ceftriaxone or other drugs are used for sepsis depending on sensitivity tests. Resistance to ampicillin and chloramphenicol is mediated by plasmid-encoded [ندعوك للتسجيل في المنتدى أو التعريف بنفسك لمعاينة هذه الصورة]-lactamases and acetylating enzymes, respectively. Prevention Public health measures, e.g., sewage disposal, chlorination of the water supply, stool cultures for food handlers, and hand washing prior to food handling. Do not eat raw eggs or meat. No vaccine is available. |
| Shigella Species (e.g., S. dysenteriae, S. sonnei) Disease Enterocolitis (dysentery). Characteristics Facultative gram-negative rods. Non-lactose-fermenting. Nonmotile, in contrast to Salmonella. Habitat and Transmission Habitat is the human colon only; unlike Salmonella, there are no animal carriers for Shigella. Transmission is by the fecal–oral route. Pathogenesis Invades the mucosa of the ileum and colon but does not penetrate farther; therefore, sepsis is rare. Endotoxin in cell wall. Infectious dose is much lower (1–10 organisms) than that of Salmonella. The infectious dose of Shigella is low because it is resistant to stomach acid. Children in mental institutions and day-care centers experience outbreaks of shigellosis. No chronic carrier state. Laboratory Diagnosis Gram-stained smear and culture. Non-lactose-fermenting colonies on EMB or MacConkey's agar. TSI agar shows an alkaline slant with an acid butt and no gas or H2S. Identified by biochemical reactions or by serology with anti-O antibody in agglutination test. Serologic tests for antibodies in the patient's serum are not done. Treatment In most cases, fluid and electrolyte replacement only. In severe cases, ciprofloxacin. Resistance is mediated by plasmid-encoded enzymes, e.g., [ندعوك للتسجيل في المنتدى أو التعريف بنفسك لمعاينة هذه الصورة]-lactamase, which degrades ampicillin, and a mutant pteroate synthetase, which reduces sensitivity to sulfonamides. Prevention Public health measures, e.g., sewage disposal, chlorination of the water supply, stool cultures for food handlers, and hand washing prior to food handling. Prophylactic drugs not used. No vaccine is available. |
| Vibrio cholerae Disease Cholera. Characteristics Comma-shaped gram-negative rods. Oxidase-positive, which distinguishes them from Enterobacteriaceae. Habitat and Transmission Habitat is the human colon. Transmission is by the fecal–oral route. Pathogenesis Massive, watery diarrhea caused by enterotoxin that activates adenylate cyclase by adding ADP-ribose to the stimulatory G protein. Increase in cyclic AMP causes outflow of chloride ions and water. Toxin has two components: subunit A, which has the ADP-ribosylating activity; and subunit B, which binds the toxin to cell surface receptors. Organism produces mucinase, which enhances attachment to the intestinal mucosa. Role of endotoxin is unclear. Infectious dose is high (>107 organisms). Carrier state rare. Laboratory Diagnosis Gram-stained smear and culture. (During epidemics, cultures not necessary.) Agglutination of the isolate with known antisera confirms the identification. Treatment Treatment of choice is fluid and electrolyte replacement. Tetracycline is not necessary but shortens duration and reduces carriage. Prevention Public health measures, e.g., sewage disposal, chlorination of the water supply, stool cultures for food handlers, and hand washing prior to food handling. Vaccine containing killed cells has limited effectiveness. Tetracycline used for close contacts. |
| Vibrio parahemolyticus Comma-shaped gram-negative rod found in warm sea water. Causes watery diarrhea. Acquired by eating contaminated raw seafood. Outbreaks have occurred on cruise ships in Caribbean. Diarrhea is mediated by enterotoxin similar to cholera toxin. |
| Vibrio vulnificus Comma-shaped gram-negative rod found in warm sea water. Causes cellulitis and life-threatening sepsis with hemorrhagic bullae. Acquired either by trauma to skin, especially in shellfish handlers, or by ingestion of raw shellfish, especially in patients who are immunocompromised or have liver damage. |
| Campylobacter jejuni Disease Enterocolitis. Characteristics Comma-shaped gram-negative rods. Microaerophilic. Grows well at 42°C. Habitat and Transmission Habitat is human and animal feces. Transmission is by the fecal–oral route. Pathogenesis Invades mucosa of the colon but does not penetrate; therefore, sepsis rarely occurs. No enterotoxin known. Laboratory Diagnosis Gram-stained smear plus culture on special agar, e.g., Skirrow's agar, at 42°C in high-CO2, low-O2 atmosphere. Serologic tests not useful. Treatment Usually symptomatic treatment only; erythromycin for severe disease. Prevention Public health measures, e.g., sewage disposal, chlorination of the water supply, stool cultures for food handlers, and hand washing prior to food handling. No preventive vaccine or drug is available. |
| Helicobacter pylori Disease Gastritis and peptic ulcer. Risk factor for gastric carcinoma. Characteristics Curved gram-negative rod. Habitat and Transmission Habitat is the human stomach. Transmission is by ingestion. Pathogenesis Organisms synthesize urease, which produces ammonia that damages gastric mucosa. Ammonia also neutralizes acid pH in stomach, which allows the organism to live in gastric mucosa. Laboratory Diagnosis Gram stain and culture. Urease-positive. Serologic tests for antibody and the "urea breath" test are useful. Treatment Amoxicillin, metronidazole, and bismuth (Pepto-Bismol). Prevention No vaccine or drug is available. |
| Klebsiella pneumoniae Diseases Pneumonia, UTI, and sepsis. Characteristics Facultative gram-negative rods with large polysaccharide capsule. Habitat and Transmission Habitat is the human upper respiratory and enteric tracts. Organism is transmitted to the lungs by aspiration from upper respiratory tract and by inhalation of respiratory droplets. It is transmitted to the urinary tract by ascending spread of fecal flora. Pathogenesis Endotoxin causes fever and shock associated with sepsis. No exotoxin known. Organism has large capsule, which impedes phagocytosis. Chronic pulmonary disease predisposes to pneumonia; catheterization predisposes to UTI. Laboratory Diagnosis Gram-stained smear and culture. Characteristic mucoid colonies are a consequence of the organism's abundant polysaccharide capsule. Lactose-fermenting colonies on MacConkey's agar. Differentiated from Enterobacter and Serratia by biochemical reactions. Treatment Cephalosporins alone or with aminoglycosides, but antibiotic sensitivity testing must be done. Resistance is mediated by plasmid-encoded enzymes. Prevention No vaccine or drug is available. Urinary and intravenous catheters should be removed promptly. |
| Enterobacter cloacae Enteric gram-negative rod similar to K. pneumoniae. Causes hospital-acquired pneumonia, UTI, and sepsis. Highly antibiotic-resistant. |
| Serratia marcescens Enteric gram-negative rod similar to K. pneumoniae. Causes hospital-acquired pneumonia, UTI, and sepsis. Red-pigmented colonies. Highly antibiotic-resistant. |
| Proteus Species (e.g., P. vulgaris, P. mirabilis) Diseases UTI and sepsis. Characteristics Facultative gram-negative rods. Non-lactose-fermenting. Highly motile. Produce urease, as do Morganella and Providencia species (see below). Antigens of OX strains of P. vulgaris cross-react with many rickettsiae. Habitat and Transmission Habitat is the human colon and the environment (soil and water). Transmission to urinary tract is by ascending spread of fecal flora. Pathogenesis Endotoxin causes fever and shock associated with sepsis. No exotoxins known. Urease is a virulence factor because it degrades urea to produce ammonia, which raises the pH. This leads to "struvite" stones, which can obstruct urine flow, damage urinary epithelium, and serve as a nidus for recurrent infection by trapping bacteria within the stone. Organism is highly motile, which may facilitate entry into the bladder. Predisposing factors are colonization of the vagina, urinary catheters, and abnormalities of the urinary tract such as strictures, valves, and stones. Laboratory Diagnosis Gram-stained smear and culture. "Swarming" (spreading) effect over blood agar plate as a consequence of the organism's active motility. Non-lactose-fermenting colonies on EMB or MacConkey's agar. TSI agar shows an alkaline slant and acid butt with H2S. Organism produces urease, whereas Salmonella, which can appear similar on TSI agar, does not. Serologic tests not useful. P. mirabilis is indole-negative, whereas P. vulgaris, M. morganii, and Providencia species are indole-positive. Treatment Trimethoprim-sulfamethoxazole or ampicillin is often used for uncomplicated UTIs, but a third-generation cephalosporin should be used for serious infections. The indole-negative species P. mirabilis is more likely to be sensitive to antibiotics such as ampicillin than are the indole-positive species. Antibiotic sensitivities should be tested. Resistance is mediated by plasmid-encoded enzymes. Prevention No vaccine or drug is available. Prompt removal of urinary catheters helps prevent urinary tract infections. |
| Morganella morganii Enteric gram-negative rod similar to Proteus species. Causes UTIs and sepsis. Highly motile and produces urease. Indole-positive and more resistant to antibiotics than P. mirabilis. |
| Providencia rettgeri Enteric gram-negative rod similar to Proteus species. Causes UTIs and sepsis. Highly motile and produces urease. Indole-positive and more resistant to antibiotics than P. mirabilis. |
| Pseudomonas aeruginosa Diseases Wound infection, UTI, pneumonia, and sepsis. One of the most important causes of nosocomial infections, especially in burn patients and those with cystic fibrosis. Causes endocarditis in intravenous drug users. Characteristics Aerobic gram-negative rods. Non-lactose-fermenting. Pyocyanin (blue-green) pigment produced. Oxidase-positive, which distinguishes it from members of the Enterobacteriaceae family. Habitat and Transmission Habitat is environmental water sources, e.g., in hospital respirators and humidifiers. Also inhabits the skin, upper respiratory tract, and colon of about 10% of people. Transmission is via water aerosols, aspiration, and fecal contamination. Pathogenesis Endotoxin is responsible for fever and shock associated with sepsis. Produces exotoxin A, which acts like diphtheria toxin (inactivates EF-2). Pili and capsule are virulence factors that mediate attachment and inhibit phagocytosis, respectively. Glycocalyx-producing strains predominate in chronic infections in cystic fibrosis patients. Strains with type III secretion systems are more virulent than those without. Severe burns and neutropenia are important predisposing factors. Laboratory Diagnosis Gram-stained smear and culture. Non-lactose-fermenting colonies on EMB or MacConkey's agar. TSI agar shows an alkaline slant and an alkaline butt because the sugars are not fermented. Oxidase-positive. Serologic tests not useful. Treatment Antibiotics must be chosen on the basis of antibiotic sensitivities because resistance is common. Anti-pseudomonal penicillin and aminoglycoside are often used. Resistance is mediated by a variety of plasmid-encoded enzymes, e.g., [ندعوك للتسجيل في المنتدى أو التعريف بنفسك لمعاينة هذه الصورة]-lactamases and acetylating enzymes. Prevention Disinfection of water-related equipment in the hospital, hand washing, and prompt removal of urinary and intravenous catheters. There is no vaccine. |
| Burkholderia cepacia Gram-negative rod resembling P. aeruginosa. Important cause of chronic infections in patients with cystic fibrosis. Formerly called Pseudomonas cepacia. |
| Stenotrophomonas maltophilia Gram-negative rod resembling P. aeruginosa. Important cause of chronic infections in patients with cystic fibrosis. Formerly called Pseudomonas maltophilia. |
| Bacteroides fragilis Diseases Sepsis, peritonitis, and abdominal abscess. Characteristics Anaerobic, gram-negative rods. Habitat and Transmission Habitat is the human colon, where it is the predominant anaerobe. Transmission occurs by spread from the colon to the blood or peritoneum. Pathogenesis Lipopolysaccharide in cell wall is chemically different from and less potent than typical endotoxin. No exotoxins known. Capsule is antiphagocytic. Predisposing factors to infection include bowel surgery and penetrating abdominal wounds. Laboratory Diagnosis Gram-stained smear plus anaerobic culture. Identification based on biochemical reactions and gas chromatography. Serologic tests not useful. Treatment Metronidazole, clindamycin, and cefoxitin are all effective. Abscesses should be surgically drained. Resistance to penicillin G, some cephalosporins, and aminoglycosides is common. Plasmid-encoded [ندعوك للتسجيل في المنتدى أو التعريف بنفسك لمعاينة هذه الصورة]-lactamase mediates resistance to penicillin. Prevention In bowel surgery, perioperative cefoxitin can reduce the frequency of postoperative infections. No vaccine is available. |
| Prevotella melaninogenica Anaerobic gram-negative rod resembling B. fragilis. Member of normal flora found primarily above the diaphragm (e.g., mouth) in contrast to B. fragilis, which is found below (e.g., colon). Often involved in brain and lung abscesses. Formerly called Bacteroides melaninogenicus. |
