Gram negative bacilli (Enterobacteriaceae)

Most medically important family of non–spore-forming gram-negative rods.
Most species are normal flora of the GI tract. Salmonella, Shigella, and Yersinia are not normal GI flora.
Major cause of nosocomial infections
Diseases include UTIs, gastroenteritis, septicemia, food poisoning, wound infections, peritonitis, pneumonia, and meningitis
The family exhibits four serological characteristics:
O (somatic) antigen-A cell wall antigen-LPS (heat stable), Used for serological grouping of Salmonella & Shigella.
K (envelope) antigen-Capsular antigen (heat labile)
H (flagellar) antigen-Flagellar antigen-protein (heat labile), Used to serotype Salmonella.
Vi antigen-Capsular antigen of Salmonella Typhi-polysaccharide (heat labile), Role in preventing phagocytosis, may mask O Ag, removed by heating.
Enterobacteriaceae are facultative anaerobes, ferment glucose. Positive nitrate and catalase, non-hemolytic. Except for Plesiomonas, they are oxidase negative.

1. Gram negative bacilli Enterobacteriaceae facultative anaerobes Escherichia spp. Klebsiella spp. Enterobacter spp. Citrobacter spp. Serratia spp. Salmonella spp. Shigella spp. Proteus spp. Morganella spp. Providencia spp. Yersinia spp.

2. General family characteristics Most medically important family of n on–spore-forming gram-negative rods . Most species are normal flora of the GI tract. Salmonella, Shigella, and Yersinia are not normal GI flora. Major cause of nosocomial infections Diseases include UTIs, gastroenteritis, septicemia, food poisoning, wound infections, peritonitis, pneumonia, and meningitis The family exhibits four serological characteristics: O (somatic) antigen-A cell wall antigen-LPS (heat stable), Used for serological grouping of Salmonella & Shigella. K (envelope) antigen-Capsular antigen (heat labile) H (flagellar) antigen-Flagellar antigen-protein (heat labile), Used to serotype Salmonella. Vi antigen-Capsular antigen of Salmonella Typhi-polysaccharide (heat labile), Role in preventing phagocytosis, may mask O Ag, removed by heating. Enterobacteriaceae are facultative anaerobes , ferment glucose. Positive nitrate and catalase, n on-hemolytic. Except for Plesiomonas , they are oxidase negative.

3. Enteric media MacConkey (MAC) agar: Lactose-positive colonies are pink/red, and lactose-negative colonies are colorless. Eosin-methylene blue (EMB) agar: Colonies of lactose fermenters have a dark center, and lactose non fermenters are colorless. E. coli has a dark center and usually shows a green metallic sheen. Hektoen enteric (HE) agar: Lactose and/or sucrose fermenters form yellow/orange colonies. Salmonella colonies are green with black centers (H2S positive), and Shigella colonies are green. Xylose-lysine- desoxycholate (XLD) agar: Colonies of lactose and/or sucrose fermenters are yellow. Salmonella produce red colonies with black centers (H2 S), and Shigella have clear colonies. Salmonella-Shigella (SS) agar: Lactose fermenters produce red colonies; Salmonella colonies are colorless with black centers, and Shigella colonies are colorless. Bismuth sulfite agar: Salmonella Typhi produces black colonies; lactose-fermenting colonies are yellow-orange. Brilliant green agar: Proteus and Salmonella species produce red/pink colonies, whereas Shigella and most lactose fermenters will not grow. Selenite broth: The broth is an enhancement medium for stool cultures. Salmonella growth is enhanced, whereas gram-positive and coliform (normal GI flora) bacteria are inhibited. It is no longer commonly used. Deoxycholate citrate agar (DCA) selective for enteric bacilli, such as Salmonella spp. and Shigella spp.

4. Escherichia coli Gram reaction & characteristics: Gram negative, LF, motile bacilli. Habitat: Normal microbiota of the bowel (GIT) of humans and other animals; may also inhabit female genital tract. Virulence factor: Endotoxin (lipid A/LPS> septic shock), capsule production, and pili that mediate attachment to host cells. Disease: Urinary tract infections (UPEC), bacteremia, septicemia, meningitis & sepsis in newborns , appendicitis, peritonitis, gallbladder infections, endocarditis, gastroenteritis, food poisoning and nosocomial infections. Pneumonia (hospitalized patients). Mode of transmission: Person-to-person, especially in health care–associated environments. Fecal-oral spread between humans in contaminated food or water or consumption of undercooked beef or unpasteurized milk from colonized cattle.

5. Lab diagnosis: Samples: urine, CSF, blood, stool, food. On Triple sugar iron (TSI): Acid over acid (A/ A) and H2S negative, gas production. On MacConkey agar: Pink/red colonies, LF. On SBA, colonies are shiny, opaque, off-white, beta-hemolytic. On EMB agar: Green metallic sheen colonies with dark centers. On CLED agar: yellow colonies. I ndole, methyl red (MR), motility, and o-nitrophenyl-13-Dgalactopyranoside (ONPG) positive. Voges-Proskauer (V P), citrate, and urease negative . Treatment: Rehydration (diarrhea); TMP-SMX, penicillin (UTI); third-generation cephalosporin (meningitis, sepsis). Note: E. coli is the most common cause of UTI and Gram - ve sepsis. Most common causes of neonatal meningitis: Group B Strep E. coli Listeria Most common causes of neonatal pneumonia: Group B Strep E. coli

6. Enterohemorrhagic E. coli (EHEC, STEC, VTEC): Virulence factor: Toxin ( Stx 1 & 2/ verotoxin ), similar to Shiga toxin produced by Shigella dysenteriae . Most frequently associated with certain serotypes, such as E. coli O157:H7. Disease: Inflammation and bleeding of the mucosa of the large intestine (i.e., hemorrhagic colitis); can also lead to hemolytic uremic syndrome (HUS), resulting from toxin mediated damage to kidneys (kidney failure in children). Transmitted by ingestion of undercooked beef ( hamburger), contaminated foods such as apple cider, basil, sprouts or raw milk. Lab diagnosis: Growth on sorbitol-MacConkey (SMAC) agar: s orbitol replaces lactose in the medium. E. coli O157:H7 does not metabolize sorbitol; most other E. coli strains rapidly ferment sorbitol, producing pink colonies on SMAC. E. coli O157:H7 colonies appear colorless on SMAC. Confirmatory testing is by detection of Stx-1 and Stx-2. HUS: hemolytic anemia (schistocytes), thrombocytopenia.

7. Other strains of E. coli causing human intestinal infections Enterotoxigenic E.coli (ETEC): Virulence factor: Pili that permit gastrointestinal colonization. Heat-labile (LT) and heat-stable (ST) enterotoxins that mediate secretion of water and electrolytes into the bowel lumen. Disease: Travelers (epidemic) and childhood diarrhea, characterized by profuse, watery stools. Transmitted by contaminated food and water. Enteroinvasive E. coli (EIEC): Invades enterocytes lining the large intestine, Dysentery (i.e., necrosis, ulceration, and inflammation of the large bowel, bloody diarrhea ); usually seen in young children living in areas of poor sanitation. From contaminated food or water. Gram stain of stool shows: polys, RBCs, mucus. Enteropathogenic E. coli (EPEC) Virulence factor: Bundle-forming pilus, intimin, and other factors that mediate organism attachment to mucosal cells of the small bowel, resulting in changes in cell surface (i.e., loss of microvilli). Disease: Watery diarrhea in infants in developing, low-income nations; can cause a chronic diarrhea. Transmitted by food contaminated with fecal material.

8. Enteroaggregative E. coli (EAEC): Virulence factor: Binding by pili, ST-like, and hemolysin-like toxins. Disease: Watery diarrhea that in some cases can be prolonged (HIV patients). Nosocomial and community acquired.

9. Klebsiella Gram reaction & characteristics: Gram negative bacilli, LF (fast fermenter), with l arge capsule gives colonies mucoid appearance, non-motile. Habitat: Gastrointestinal microbiota. Virulence factor: Endotoxins, capsules, adhesion proteins, and resistance to multiple antimicrobial agents. Disease: Health care–associated infections of the respiratory tract ( pneumonia- bloody “currant-jelly” purulent sputum ) , nosocomial UTI, septicemia , wound infection, meningitis, endocarditis. Most commonly infect hospitalized and seriously debilitated patients, d iabetics and alcoholics. The most common species isolated is K. pneumoniae (Friedlander bacillus). Mode of transmission: Endogenous or person-to-person spread, especially in hospitalized patients.

10. Lab diagnosis: Samples: urine, blood, pleural fluids & wounds. Culture: MAC: pink, LF, mucoid because of capsule production. CLED: yellow. EMB: pink-purple. Biochemical test: Positive: catalase, citrate, nitrate reduction, TSI: A/A with gas, urease (slow), VP. Motility & ODC differentiate from Enterobacter , indole except ( for K. oxytoca and K. ornithinolytica ), Treatment: Third-generation cephalosporin. Carbapenems (imipenem) effective against ESBL strains.

11. Enterobacter Gram reaction & characteristics: Gram negative bacilli, LF, motile. Habitat: Normal human gastrointestinal microbiota. Virulence factor: Endotoxins, adhesion proteins, and resistance to multiple antimicrobial agents. Disease: Health care–associated infections of the respiratory tract, urinary tract, blood, and several other normally sterile sites; most commonly infect hospitalized and seriously debilitated patients. E. cloacae is the most common, and E. aerogenes is the second most common species isolated. Mode of transmission: Endogenous or person-to-person spread, especially in hospitalized patients.

12. Lab diagnosis: Samples: urine, blood. Culture: MAC: pink. CLED: yellow. EMB: pink-purple. Biochemical tests: Positive: VP, gas, motility, ODC and citrate, catalase, Negative: H2S, MR, and indole, oxidase. Ferment glucose, lactose. All species except E. taylorae are lactose positive. E. aerogenes is arginine negative and lysine positive. E. cloacae is arginine positive and lysine negative. Treatment: Carbapenems, beta-lactamase inhibitors, fluoroquinolones, aminoglycosides, fourth generation cephalosporins & sulfamethoxazole/trimethoprim (TMP-SMZ). Note: colonies of Enterobacter may be mucoid. Same IMViC reactions as Klebsiella. Enterobacter are motile.

13. Citrobacter Gram reaction & characteristics: Gram negative bacilli, Habitat: Normal human gastrointestinal microbiota. Virulence factor: Endotoxins, adhesion proteins, and resistance to multiple antimicrobial agents. Disease: Health care–associated infections of the respiratory tract, urinary tract, blood, and several other normally sterile sites; most commonly infect hospitalized and seriously debilitated patients. Nosocomial infections . C. freundii is the most common species isolated. Mode of transmission: Endogenous or person-to-person spread, especially in hospitalized patients.

14. Lab diagnosis: Samples: urine, blood, stool. Culture: MAC: colorless or slightly pink color (slow/weak LF). HE: colorless. XLD: red/colorless or yellow, with or without H2S. SS: colorless with or without black centers. C. freundii resembles E. coli on MAC but can be differentiated because of being H2S (+) and indole (-). Biochemical tests: Positive: Gas, H2S, MR, citrate, motility, ONPG. Lactose variable. ONPG & LDC differentiate from Salmonella. A/AG H2S reaction in KIA. Treatment: Cefepime.

15. Serratia Gram reaction & characteristics: Gram negative bacilli, weak LF. Habitat: Normal human gastrointestinal microbiota. Virulence factor: Endotoxins, adhesion proteins, and resistance to multiple antimicrobial agents. Disease: Health care–associated infections of the respiratory tract, urinary tract, blood, and several other normally sterile sites; most commonly infect hospitalized and seriously debilitated patients, causes opportunistic infections ( Pneumonia & septicemia, meningitis) in patients undergoing chemotherapy and immunosuppressed patients. S. marcescens is the most common clinical isolate. Mode of transmission: Endogenous or person-to-person spread, especially in hospitalized patients.

16. Lab diagnosis: Samples: urine, blood, sputum, CSF. Culture: MAC: colorless or slightly pink color after 24-48 hours. EMB: pink-purple. HE: colorless. XLD: yellow or colorless. CLED: Some strains produce a brick-red pigment (prodigiosin), which is enhanced with room temperature incubation. Biochemical tests: Positive: DNase, gelatinase, lipase, VP, motility, citrate, catalase, urease, ONPG positive but a delayed lactose fermenter. TSI: A/A. Treatment: Third generation cephalosporins. Imipenem, meropenem.

17. Salmonella Gram reaction & characteristics: Gram negative, bacilli, NLF, motile. Habitat: Only found in humans but not part of normal microbiota of the bowel. Virulence factor: Pili, attachment and phagocytosis by intestinal mucosal cells, allow survival in and destruction of phagocytes, and facilitate dissemination to other tissues. Endotoxin, S. t yphi produces virulence (Vi) antigen (protect against complements). Disease: The majority of human cases of salmonellosis are due to serotypes belonging to the species S. enterica, which includes the serotype S. Typhi. S. typhi: typhoid (enteric) fever, enterocolitis, salmonella bacteremia, the most severe form. S. paratyphi A, b and C: Paratyphoid fever, Salmonella bacteremia. Salmonella typhimurium & Salmonella enteritidis: Salmonella gastroenteritis. Salmonellosis (diarrhea, fever, and abdominal cramps). Less common manifestations, especially in immunocompromised patients, are osteomyelitis (SCA), meningitis, UTI, and septicemia. Mode of transmission: Person-to-person spread by fecal-oral route. By ingestion of food (eggs, unpasteurized milk, poultry) or water contaminated with human excreta.

18. Lab diagnosis: Samples: stool, blood, BM, urine, CSF, sputum. Culture: MAC: except S. typhi, all are colorless (vs E. coli). EMB: colorless. HE: blue-green with or without black centers. SSA: colorless + black centers. DCA: colorless with H2S. XLD: red + black centers. Wilson and Blair’s bismuth sulfite agar: especially S. typhi, Shigella spp., Proteus spp., and coliforms is inhibited on this medium. salmonellae produce jet black colonies surrounded by a metallic sheen due to production of hydrogen sulphide . S. Paratyphi A and other species, which do not produce H2S, form green colonies. Most salmonellae except S. Paratyphi A, produce H2S. Biochemica l test: H2S, motility, MR, LDC and citrate positive Indole, urease (vs proteus), and lactose negative. Most Salmonella isolates produce a K/AG + H2S reaction on TSI and KIA. Most species produce gas in glucose-containing media (Salmonella serotype Typhi does not). Salmonella serotype Typhi usually produces a K/A reaction, with only a small amount of blackening (H2S production) at the site of the stab and within the stab line.

19. Lysine iron agar is a useful screening medium, because most Salmonella isolates are lysine decarboxylase positive and produce H2S. Most species produce lysine and ornithine decarboxylase (Salmonella serotype Typhi does not produce ornithine decarboxylase). Treatment: Ceftriaxone for resistant strains. Ciprofloxacin, ampicillin for carriers. Cholecystectomy may be necessary for carriers. Two oral vaccines (killed or live-attenuated) available for travelers.

20. Shigella Gram reaction & characteristics: Gram negative bacilli, NLF & non-motile. Habitat: Only found in humans at times of infection; not part of normal microbiota. Virulence factor: Shiga toxin , adherence and invasion of mucosal cells, escape from phagocytic vesicles, intercellular spread, and inflammation. Disease: Dysentery ( shigellosis or bacillary dysentery) , acute inflammatory colitis and bloody diarrhea) characterized by cramps; tenesmus, and bloody; mucoid stools. Infections with Shigella sonnei may produce watery diarrhea. Highly pathogenic; Less than 50 bacteria can cause disease. Mode of transmission: Four Fs for transmission: fingers, flies, food, feces. Person-to-person spread by fecal-oral route ( food poisoning) , especially in overcrowded areas, group settings (e.g., daycare, jails, prisons) and areas with poor sanitary conditions.

21. O antigen: polysaccharide in outer membrane used to classify Shigella genus into 4 groups S. dysenteriae (serogroup A) produces an enterotoxin, which affects the large intestines, and a neurotoxin that may result in paralysis. S. dysenteriae is mannitol and ONPG negative. S.fiexneri (serogroup B) produces a mild diarrhea. It is mannitol positive and ONPG negative. S. boydii (serogroup C) produces a mild diarrhea. S. boydii is mannitol positive and ONPG negative. It is difficult to biochemically distinguish S. flexneri from S. boydi . S. sonnei (serogroup D) produces a mild diarrhea. It is the most common cause of shigellosis in the U.S. S. sonnei is mannitol and ONPG positive. It is a delayed lactose fermenter.

22. Lab diagnosis: Samples: stool, food. Culture: Selenite F broth, tetrathionate broth, GN broth (selectivity). MAC: colorless. EMB: translucent or colorless. XLD: red or colorless. DCA: colorless, if prolonged (LF/pink). SSA: colorless- translucent, or transparent. Hektoen enteric agar (HE): green. Biochemical test: MR, nitrate positive. Catalase positive except S. dysenteriae type 1. No H2S production & non-motile (vs salmonella), negative VP, LDC, citrate & urease. L actose non-fermenter except S. sonnei (delayed LF). TSI & KIA: (K/A). Treatment: Oral rehydration for moderate cases. Fluoroquinolones for severe cases. Note: Shiga toxin, similar to Shiga-like toxins produced by EHEC, can cause HUS .

23. Proteus Gram reaction & characteristics: Gram negative bacilli, NLF, Pleomorphic, motile. Habitat: Normal human gastrointestinal microbiota, soil, water, sewage. Virulence factor: Endotoxins, adhesion proteins, and resistance to multiple antimicrobial agents. Disease: Health care–associated infections. UTI (triple phosphate/ ammonium magnesium phosphate or struvite stones , alk aline urine ), ear & wound infections, septicemia, respiratory infection (pneumonia ) , meningitis, burn infection (hospital acquired), septicemia. Proteus vulgaris and P. mirabilis are the most common isolates. Mode of transmission: Endogenous or person-to-person spread, especially in hospitalized patients.

24. Lab diagnosis: Samples: urine, blood, CSF, wounds (pus). Culture: MAC: colorless. CLED: NLF, no swarming. EMB: colorless. HE: blue-green+H2S. XLD: red/colorless or yellow (some)+H2S. BA,CHOC: P. mirabilis and many strains of P. vulgaris exhibit swarming motility on SBA. Burned chocolate or fishy odor, or seminal odor. Biochemical tests: Positive: H2S, MR, motility, urease (vs salmonella), tryptophan deaminase (TDA), and phenylalanine deaminase (PAD). TSI & KIA: K/A with or without H2S. P. mirabilis is indole negative; P. vulgaris is indole positive. Treatment: TMP-SMX. Ampicillin. Note: T he Weil-Felix reaction uses Proteus vulgaris antigens (O Ag) to diagnose Rickettsia. The Proteus antigens cross-react with a patient’s serum antibodies against Rickettsia.

25. Morganella morganii proteus morganii Gram reaction & characteristics: Gram negative bacilli, NLF, aerobic, motile. Habitat: Normal human gastrointestinal microbiota. Virulence factor: Endotoxins, adhesion proteins, and resistance to multiple antimicrobial agents. Disease: Mainly nosocomial infections. UTI, wound infections, genitourinary infections, septicemia, meningitis, diarrhea. Mode of transmission: Endogenous or person-to-person spread, especially in hospitalized patients.

26. Lab diagnosis: Samples: urine, CSF, blood. Culture: Blood agar: no swarming. MacConkey, HE: colorless. XLD: red or colorless. CLED: NLF. EMB: colorless. Biochemical tests: Positive: PDA and TDA, Indole, MR, urease, ODC. K/AG reaction on TSI and KIA; H2S negative. Treatment: Cefepime, imipenem, meropenem, piperacillin, aminoglycosides & fluoroquinolones.

27. Providencia stuartii Gram reaction & characteristics: Gram negative bacilli, NLF & motile. Habitat: Normal human gastrointestinal microbiota. Virulence factor: Endotoxins, adhesion proteins, and resistance to multiple antimicrobial agents. Disease: The most common isolate is probably P. stuartii & P. rettgeri . UTI, diarrhea. Most common cause of UTI in nursing home patients with indwelling catheters. Septicemia, pneumonia. Wounds infection, meningitis. Mode of transmission: Endogenous or person-to-person spread, especially in hospitalized patients.

28. Lab diagnosis: Samples: urine, stool, blood, throat, perineum, axilla, wounds. Culture: Blood agar: no swarming. Nutrient agar: shiny colonies. MacConkey, HE agar: colorless XLD: yellow or colorless. CLED: NLF. EMB: colorless. Fruity smell and on DCA form yellow to orange colonies. Biochemical test: Positive: PDA, TDA, indole, MR , citrate, nitrate reduction, fermentative (glucose). K/A reaction on TSI and KIA, with or without gas (usually without); H2S negative . Only P. rettgeri hydrolyses urea. Treatment: Aztreonam, carbapenems.

29. Note: Proteus, Morganella , and Providencia spp. are the only members of the Enterobacteriaceae family that produc e phenylalanine deaminase (PDA). Strong positive urease results are produced by Proteus, Morganella , and Providencia spp., where a weak positive urease results are produced by Klebsiella spp. And some Enterobacter spp. The swarming of proteus spp. Is inhibited by: Agar in the medium from 1–2% to 6%, culture on MAC (bile salt), CLED. Chloral hydrate, sodium azide , alcohol (56%), sulfonamide, boric acid.

30. Y ersinia spp Gram reaction & characteristics: Gram negative bacilli, NLF, capsulate at 37C. Wayson stain or MB, Giemsa, Wright, bipolar staining resembling safety pin. Habitat: Y. pestis: carried by urban and domestic rats and wild rodents, such as the ground squirrel, rock squirrel, and prairie dog. Y. enterocolitica: d ogs, cats, rodents, rabbits, pigs, sheep, and cattle. Y. pseudotuberculosis: r odents, rabbits, deer, and birds. Virulence factor: Y. pestis: intracellular survival and production of an antiphagocytic capsule, exotoxins, endotoxins, coagulase, and fibrinolysin. Y. enterocolitica & Y. pseudotuberculosis: virulence plasmid allow the organism to attach to and invade the intestinal mucosa and spread to lymphatic tissue. Disease: Y. pestis: is considered a potential bioterrorism agent . The plague (black death), dark black skin patches (endotoxin causes DIC → cutaneous hemorrhagic necrosis causing black color. Bubonic plague: high fever and painful inflammatory swelling of axilla and groin lymph nodes, buboes. Bacteremia. Pneumonic plague: involves the lungs.

31. Y. enterocolitica: Enterocolitis characterized by fever, bloody diarrhea, and abdominal pain; also can cause acute mesenteric lymphadenitis, which may present clinically as appendicitis (i.e., pseudoappendicular syndrome). G astroenteritis, peritonitis, bacteremia and abscess . Most common complication is arthritis. Y. pseudotuberculosis: Y. pseudotuberculosis is a rare cause of acute mesenteric lymphadenitis, septicemia in children. Mode of transmission: Y. pestis: R odents to humans (bite of flea vectors), ingestion of contaminated animal tissues, person-to-person by inhalation of contaminated airborne droplets (pneumonic). Y. enterocolitica: Consumption of incompletely cooked food products (especially pork), dairy products such as milk, and, less commonly, by ingestion of contaminated water or by contact with infected animals. Y. pseudotuberculosis: Ingestion of organism during contact with infected animal or from contaminated food or water.

32. Lab diagnosis: Samples: sputum, blood, stool culture, culture of bubo fluid, pus. Presumptive identification of Y. pestis is based on isolation of the bacterium from respiratory tract, blood, or lymph nodes (ASM). Culture: Optimal growth temperature: 25-30C. Y. pestis: BA, CHOC: grey-white, non-hemolytic. Fried egg or hammered copper appearance  ( older cultures). MAC: colorless. In undisturbed broth cultures, Y. pestis grows in clumps (cotton fluff) that are described as flocculent or stalactite in appearance. The term stalactite refers to icicle-like calcium carbonate deposits that hang down from the roofs of caves. Y. enterocolitica: MAC: colorless. HE: salmon. XLD: yellow or colorless. Cefsulodin - Irgasan - novobiocin (CIN) medium is a selective and differential medium for the isolation and differentiation of Yersinia spp. Y. enterocolitica colonies have a bulls-eye appearance (a red center surrounded by a transparent zone). Y. pseudotuberculosis does not produce bulls-eye colonies.

33. Biochemical tests: Y. pestis: Catalase: Positive . Oxidase, Urease, and Indole: Negative. TSI: K/A. Y. enterocolitica : ONPG positive but delayed lactose fermenter and sucrose positive . A/ A on TSI. MR, urease. Y. pseudotuberculosis: Urease positive. All species except Y pestis are nonmotile at 37° C but motile at 25° C. Y. pestis is nonmotile at both temperatures. Treatment: Y. enterocolitica: Self-limiting. Gentamicin or chloramphenicol for septicemia. Y. pestis: Streptomycin, gentamycin, tetracycline Vaccine: killed and attenuated vaccines available, generate antibodies against F1 antigen. Note: Yersiniosis: infection by Y. enterocolitica & Y. pseudotuberculosis. Note: Biosafety Level 2 agent. BSL-3 practices and facilities for manipulations with a high potential for aerosol or droplet formation. Vaccination is available and recommended for anyone working with Y. pestis –infected rodents and other highly infectious material.

34. Alyazeed Hussein, BSc, SUST This has been a presentation of Alyazeed Hussein Thanks for your attention and kind patience @elyazeed7 @Alyazeed7ussein