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 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.

3. Enteric media
1. MacConkey (MAC) agar: Lactose-positive colonies are pink/red, and lactose-negative colonies are
colorless.
2. 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.
3. 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.
4. 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.
5. Salmonella-Shigella (SS) agar: Lactose fermenters produce red colonies; Salmonella colonies are
colorless with black centers, and Shigella colonies are colorless.
6. Bismuth sulfite agar: Salmonella Typhi produces black colonies; lactose-fermenting colonies are
yellow-orange.
7. Brilliant green agar: Proteus and Salmonella species produce red/pink colonies, whereas Shigella
and most lactose fermenters will not grow.
8. 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.
9. 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.
• Indole, 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: sorbitol 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 large 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,
diabetics 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.

14. 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.

15. • 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.

16. 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.

17. • 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.

18. 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. typhi 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.

19. • 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.
Biochemical 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.

20. • 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.

21. 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.

22. O antigen: polysaccharide in outer membrane
used to classify Shigella genus into 4 groups
1. 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.
2. S.fiexneri (serogroup B) produces a mild
diarrhea. It is mannitol positive and
ONPG negative.
3. 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.
4. 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.

23. • 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.
Lactose 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.

25. 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, alkaline 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.

26. • 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:
• The 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.

28. 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.

29. • 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.

30. 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.

31. • 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.

32. • Note: Proteus, Morganella, and Providencia spp. are the only members of the Enterobacteriaceae
family that produce 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.

33. Yersinia 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: dogs, cats, rodents, rabbits, pigs, sheep, and cattle.
• Y. pseudotuberculosis: rodents, 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.

34. • 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).
• Gastroenteritis, 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:
• Rodents 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.

35. • 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.

36. • 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.

41. Alyazeed Hussein, BSc, SUST
This has been a presentation of Alyazeed Hussein
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