med microbio--MODULE 10. ENTEROBACTERIACEAE (GRAM NEGATIVE RODS)

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97 Terms

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Enteric=

family, genus, or species level

relating to or occurring in the intestines (family is composed of several genre)

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Opportunistic Enterobacteriaceae=

  • cause disease? or normal flora?

  • found where

  • predom reside where

  • commonly referred to as ___ bac bc of where they reside

  • Most enterics do not cause disease when confined to the intestinal tract of a normal host, therefore are nonpathogenic→many are normal flora of intestines; however, if given an environment where there is a dysfunctional host response or an opportunity to invade other body sites, many enterics have the capability of producing disease in any tissue.

  • “Opportunisitic pathogens” like E. coli getting into urinary tact

  • Found in soil, water, decaying matter semicolon test by cultures, the major indicator of cleanliness and water is number of E. coli per milliliter

  •  composed of a large number of closely related bacterial genre and species that inhabit the lower alimentary canal, which is predominantly the intestinal tract of man as normal flora

  •  because of their normal habitat and man, they have been referred to as enteric/intestinal bacteria

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Enteropathogenic enterobacteriaceae=

  • why important to man

  • salmonella is causitive ag of __

  • shigella—

  • yersina—

some members of enteric bac group are among the most important intestinal pathogens of man such as salmonella– causative agent of typhoid fever, shigella-- bacillary dysentery, Yersina– the plague

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at sites external to GI, enterobac are

  • Enterobacteriaceae can be pathogenic at sites external to the GI tract

    • Can be normal flora, but become pathogens if enter external sites

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E. coli

  • e stands for

  • O2 met

  • normal flora? what % of time

  • opportunistic or pathogenic (5 diseases can or does cause)

  • lactose __=strains of concern

  • can produce___toxin

  • sero strain ___:__ “enterohemorrhagic E.coli” or EHEC—>2 antigens used to ID

  1. (E=escherichiaeae genus→Escherichia coli)

  • Predominant facultative organism that makes up the normal flora (95% of the time) of the large intestine

  •  opportunistic enteric rod that can cause intestinal as well as extraintestinal infections 

    • UTI, gram neg sepsis, meningitis, wounds, pneumonia

  • Lactose neg strains of of concern

  • Can produce enterotoxin 

  • Can be the serologic strain O157:H7 (O antigen and H antigen so flagella and gram neg cell wall LPS)

    • “Enterohemorrhagic E. coli” or EHEC

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other pathogenic strains of E. coli (4)

  • if toxin is prob, fever or no?

  • all are lactose __

  • symptom progression

  1. Can be other pathogenic strains: all have diff numbers after O157:__

  • EPEC (enteropathogenic E. coli)

  • ETEC (enterotoxic E. coli)

  • EIEC (enteroinvasive E. coli)

  • EaggEX (enteroaggregative E. coli primarily causing chronic diarrhea in HIV patients)

  • If toxin is a problem (EHEC, ETEC) no fever present, if just infection (EIEC, EPEC) fever present

  • All are lactose neg

  • ingestion, then 3-4s before symps of abdominal cramps and nonbloody diarrhea, then 1-2 days until bloody diarrhea, the 5-7 days until resolution (95%) or HUS – hemolytic uric syndrome (5%)-->more treatment needed

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Shiga-toxin producing E. coli O157:H7 (EHEC): 

  • important where geo

  • endo or exotoxin

  • disease comp 0157:H7 is dev of ___, which results…% death and …%____disease

  • transmitted primarily by

  • toxin effects on blood vessels/body

  • Important pathogen in North America

  •  produces Shiga toxin (exotoxin) which is the same toxin as in produced by shigella dysenteriae hence the name

  •  most important disease complications of E coli 0157:H7 is development of hemolytic uremic syndrome (HUS)

    •  occurs in 5 to 10% of patients with the strain and results in 5% death or 30% chronic renal disease 

  • Infection is transmitted primarily by food, water, direct contact with bacteria like swimming in contaminated water

  •  implicated food products are ground beef, salami, raw milk, Alfalfa sprouts, unpasteurized apple cider and apple juice, contaminated pork, poultry, lamb, bagged fresh spinach

  • toxin damages capillary lining→ platelets clump in the area to stop blood loss and initiate healing →platelets form mesh and capillaries causing damage to RBCs which prevents adequate blood flow to affected organs→ results in organ dysfunction or failure due to 85% occlusion of blood vessel 

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lab ID of Shiga-toxin producing E. coli O157:H7 (EHEC)—>3 ways (2 assays

  • Lab ID is easily performed with specialized media,

  • PCR (for fast turnaround time),

  • agglutination reactions (that are antibody-antigen assays), enzyme linked immunosorbent assay (ELISA) testing stool culture→ using antibody against toxin specifically to ID antigen in stool specimen

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Treatment of E.coli clinical infections: (antibi and symp management)

  • Antibiotics (E.coli susceptible to most but some rez emerging)

  • Fluid and electrolyte management is best treatment of diarrhea→replacing is of gravest concern and usually if done properly will ensure full recovery

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Name the most common extraintestinal infection caused by organisms from the family Enterobacteriaceae.

UTI (90%)

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Name the most common cause (genus, species) of urinary tract infection.

  • normal flora where

  • sero strain most common

  • lactose test

  • toxin prod

E. coli (E=escherichiaeae genus→Escherichia coli)

  • Predominant facultative organism that makes up the normal flora (95% of the time) of the large intestine

  •  opportunistic enteric rod that can cause intestinal as well as extraintestinal infections 

    • UTI, gram neg sepsis, meningitis, wounds, pneumonia

  • Lactose neg strains of of concern

  • Can produce enterotoxin 

  • Can be the serologic strain O157:H7 (O antigen and H antigen so flagella and gram neg cell wall LPS)

    • “Enterohemorrhagic E. coli” or EHEC

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5.     Relating to Enterobacteriaceae in general:

         a.     Describe the Gram stain morphology

b.     Describe determinants of pathogenicity in the family Enterobacteriaceae. (4)

a. gram neg rod

b. Some have capsules, flagella, LPS or endotoxin, enterotoxin (usually w/ food poisoning)

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Name 7 biochemical properties common to ALL genera within the family.

  • gram stain, O2 use, CTA sugars, oxidase, nitrate, spore formation, lactose tests

  • name of test strips that can do many biochem rxns at once

  1. Are gram-negative rods in a Gram stain

  2.  are facultative anaerobes (either for O2 req)

  3.  utilize a glucose fermentatively with release of acid and products (glucose pos in CTA sugar test)

  4.  are oxidase negative– lack cytochrome oxidase (all Neisseria is pos)

  5.  are nitrate positive– reduces nitrates to nitrites

  6.  do not produce spores 

  7. *lactose neg (lactose fermenters/pos being nonpathogenic strains of enterobac/ normal flora→ pink on MacConkey agar)= is only true for pathogenic intestinal tract bac, not other locations

  • Can use API strips to test many diff reactions

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Name the key biochemical property, which distinguishes pathogenic intestinal (enteric) bacilli from normal flora intestinal (enteric) bacilli.

(4 selective/differential media used)

Lactose fermentation: pathogens all don’t ferment lactose (Macconkey, EMB-eosin methylene blue, HE-hektoen enteric, or XLD-xylose lysine deoxycholate agar are selective and differential media to show this)

<p><span style="background-color: transparent; font-family: &quot;Times New Roman&quot;, serif;">Lactose fermentation: pathogens all don’t ferment lactose (Macconkey, EMB-eosin methylene blue, HE-hektoen enteric, or XLD-xylose lysine deoxycholate agar are selective and differential media to show this)</span></p>
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List the three major components of the enteric bacterial cell that are used in serological typing. Describe serological typing of bacteria to include isolates that are usually typed using this method and why typing is important.

  • 3 antigens used

  • analogous to what subspeciation typing

  • why important

  • Analogous to bacteriophage typing performed on staphylococcus, enteric bacterial pathogens are subspeciated using serological or antibody based typing

  •  this typing is especially useful for salmonella, shigella, shiga toxin producing E. coli, yersinia, campylobacter, vibrio (salmonella ID by O serotyping→pos for O and H antigen means agglutination/pos on macro agglutination test)

  • Serotyping of enteric pathogens is important for epidemiology and classification purposes 

Antigens used:

K–Capsular or polysaccharide antigen, only used if bacteria produces capsule, best known as Vi antigen of salmonella typhi (has role in pathogenesis of typhoid fever)

H–Flagella or protein antigen, species bacteria and genre salmonella and Arizona 

O–Somatic (relating to the body) antigen, use for epidemiologic serological subgrouping, lipopolysaccharide (LPS) also known as o antigen in the bacterial cell wall is in LPS endotoxin of gram-negative bacteria

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Endotoxin:

  • definition

  • % patients develop shock and mortality rate range

  • 3 symps/disease states in the progression of effects of endotoxin

  • why does it lead to diff consequences?

  • 3 consequences of toxin due to inflam response

LPS (gram neg) toxin released upon cell death

  • 30% of patients with enteric septicemia will develop shock with 40 to 90% mortality

  •  mechanism of endotoxin effects are not completely elucidated, however, the defect is inadequate blood supply to vital organs which causes

  1.  hypoxia - oxygen deficiency in the tissue

  2.  metabolic failure - failure of a metabolic process, maybe limited to lungs for example or one other organ

  3.  multiple organ failure - current leading cause of death and intensive care units, more organs involved means worse prognosis for patient, follows metabolic failure of one organ usually

  • Activates inflammation in multiple different ways which can lead to many different consequences ultimately leading to fever, disseminated intravascular coagulation/DIC (clotting of vasculature over the body), shock

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Enterotoxins

  • def

  • specific for cells in the ___that cause…

  • ___can be used for identification

  • 2 virulence factors in addition

exotoxin that affects intestinal tract (gram pos or gram neg can have)

  •  toxins specific for cells in the intestinal mucosa that cause gastrointestinal upset such as cramps, diarrhea, and nausea

  •  exert the toxic effect on the intestinal tract:

    •  cause transudation into the ilium (that is, passage of fluid through a membrane or tissue surface to the ileum, a region between the small and large intestines)

    •  results and diarrhea and vomiting

  •  serologic antigens specific for the enterotoxin, can be used for identification

  •  capsules and biofilms

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Define the terms selective, non-selective, enriched and differential in terms of culture media and cite examples of each.

  • nonselective vs selective exs

  • At sites external to the GI tract but with enterobacteriaceae, these samples are inoculated onto general, enriched (if not abundant yet to enhance growth of pathogen), selective and/or differential media depending on the location of the body from which the sample was taken

  • Enterobacteria from fecal samples need to be differentiated from one another since the GI tract has a lot of normal bacteria flora, many of which belong to this family

  •  and enterobacteria normal flora and pathogenic are not distinguishable when grown on nonselective (BAP) media–all look same

    • Pathogenic bacteria and stool samples are all lactose negative so microbiologists look for lactose negative colonies 

    • MacConkey agar: not pink is lactose pos (pathogen) and if H2S pos, salmonella bc only one that is→ one selective and differential media plate can give lots of info)

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Describe the morphology of Shigella and Salmonella when Gram stained.

Gram neg rod

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State the disease caused by Shigella and identify which species cause the disease.

All species cause bacillary dysentery (shigellosis)

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all Shigella specices are human_____(normal flora or pathogens)

pathogens

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Shigella species diff (2 ways)

  1. Shiga’s bacillus

  2. Boyd’s bacillus

  3. Flexner’s bacillus

  4. Sonne-Duval bacillus =>___% of shigella reported in US

(include letter of species type)

Species are differentiated serologically and biochemically:

  1. S. dysenteriae (A)- Shiga’s bacillus

  2. S. boydii (C)- Boyd’s bacillus

  3. S. flexneri (B)- Flexner’s bacillus

  4. S. sonnei (D)- Sonne-Duval bacillus =>60-80% of shigella reported in US

  • Diff letters are from typing of species

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Clinical infection shigella (all species cause 2 things, source, transmission)

  • All shigella species cause severe diarrhea and bac dysentery

  • Source is human

  • Transmission is ingestion of contam food or water

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List the three categories of disease caused by Salmonella.

  • causitive agent, source, transmission, % chronic carriers of most severe form of disease

  1. Enteric fevers are due to salmonella invading extraintestinal tissues

    1. Have typhoid fever as most severe form of disease

    2. Caused by S. typhi

    3. Source=man (only known host for S. typhi)

    4. transmission=fecal/oral route 

      1. Occurs when noninfected indiv ingest food or water fecally contam by diseased indiv or carriers

    5. 3-5% of typhoid patients (symp or asymp) develop into chronic carriers and are sources of infections for others

  2. Acute gastroenteritis is a type of food associated infection

  3. Septecemia

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3 week course of enteric fever (salmonella)

  • week 2 two phases

WEEK 1 ENTERIC FEVER manifestations: constipation>diarrhea is the rule

  • During this time, the salmonella are penetrating the intestinal wall, infecting the lymphatic system, multiplying intracellularly in host cells, being carried to the mononuclear phagocyte system (MPS: formerly known as RES) by the bloodstream where phagocytosis occurs in the lymphatics and MPS

WEEK 2: when symp really start manifesting

  • Bac re-enter the bloodstream, bacteremia dev, bac lyse, endotoxin released, patient becomes severely ill

    • Fever of 104 deg F (40 deg C)

    • Delirious

    • Abdomen is tender

    • Abdomen has rose colored spots that appear (*unique symp that look for ID and begin to look for how to tret)

  • Salmonella then reinfects the intestinal tract

    • Diarrhea

    • Necrosis (cell death that is so fast, accumulates bc don’t have enough time to remove by normal mech) and sloughing of intestinal lining

    • Intestinal ulceration develops (open wounds/sores)

WEEK 3: 

  • Patient remains febrile

  • Patient shows improvement if no complications develop (often do)

COMPLICATIONS: Most deaths associated with typhoid fever are due to complications

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complications enteric fever (3)

COMPLICATIONS: Most deaths associated with typhoid fever are due to complications

  •  severe bleeding due to necrosis of blood vessels during the ulceration process

  •  perforation of intestinal wall due to extensive ulceration

  •   Cholecystitis 

    •  inflammation of the gallbladder due to presence of salmonella

    •  bacteria may be found in the gallbladder years later

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salmonella GASTROENTERITIS manifestations:

  • when infection occurs after incub

  • how long symp last

  • 3 symp

  • most common causative agent

  • Intestinal infection usually occurring about 18 hr after ingestion of the organism

    • Since food infection, not food poisoning (faster prez), takes time to replicate

  • Disease symp are diarrhea, fever, abdominal pain

  • Usually self-limiting (lasts 2-5 days)

  • Complications: dehydration, electrolyte imbalance are major threats

  • All species of salmonella are capable of producing gastroenteritis, however most common agent is salmonella enteritidis ssp typhimurium 

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salmonella SEPTICEMIA manifestations:

  • 3 symp

  • complications

  • causitive agent

  • Fever, chills (both bloodstream related), anemia (dec RBC)

  • Complications: lesions develop systematically producing osteomyelitis, pneumonia, pulmonary abscesses, meningitis, endocarditis

  • Causative agent: salmonella cholerae-suis

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Classify Shigella and Salmonella on the basis of lactose fermentation.

Since both are pathogenic enteric species, both are lactose negative

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Discuss the relationship of somatic (O) antigen and capsular (K) antigen in the serologic typing of Shigella and Salmonella.

  • what antigen is used in typing

  • All shigella possess O antigen (LPS endotoxin from gram neg): some possess K (capsular) antigen

  •  only O antigen is used in shigella typing

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Describe antigen interference in terms of capsular (K) antigen in Shigella.

false__ test for antigens

Antigen interference: K antigen is not significant in typing shigella but may mask the O antigen (somatic) and therefore must be removed from typing 

  • Sticky K antigen therefore can cause pos antigen testing for O when there is not (false pos)

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Describe how one would proceed in typing Shigella despite the presence of antigen masking.

→K antigen is heat labile and O is heat stable so boiling bac suspension removes the K antigen interference so that typing for O can be done

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Name the most common causative agent (genus, species, serotype) of Salmonella food infection.

Tribe: salmonelleae 

  • Salmonella, Citrobacter, Arizona were formally classified as different genre within the tribe→ changes in classification and nomenclature due to DNA sequencing have caused reclassification of the genus Citrobacter into its own tribe Citrobacteriaceae and reclassification of Arizona as subspecies of salmonella

  • Includes intestinal (enteric) pathogens of the genus salmonella and enteric opportunist of the genre Citrobacter and Arizona

  • Members of genus salmonella (salmonella, citrobacter, arizona) are causative agents of salmonellosis

    • Major site of infection is the lining of the intestinal tract

    • Many strains in this genus has the potential to produce disease

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Arizona subgroup of salmonella

  • how common is it isolated from man

  • man is ____host

  • most common symp of Arizonia infect (as well as others)

  • opportunist or obligate path

  •  Used to be genus on own, now subspecies

  • Rarely isolated from man

  • Usually isolated from reptiles and birds

  • Man is an accidental host, esp of infants or immunocompromised indv

  • “Opportunist”

    • Gastroenteritis–one of most common symp of Arizona infect

    • Perionitis, pleuritis, osteomyelitis, meningitis may be caused but as less common than gastroenteritis

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Citrobacter

  • Two species of med importance:

  • Both species are causative agents of ___ (most common presentation), and 3 more

  • C. freundii and C. diversus

  • Both species are causative agents of UTI (most common presentation), wound infections, bacteremia, meningitis (pos spinal fluid cultures)

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Shigella progression of pathogenesis (4 main steps and is bac found in bloodstream? how does it evade neutrophils)

invasive organism (not toxin so fever)

  • Shigella is an invasive bacteria that enters a small intestine where it multiplies

  • it then proceeds to the mucus surface of the terminal ileum and colon

  •  bacteria multiply in the epithelial cells

  •  it invades the epithelial cells where it resides and causes abscess formation and sloughing of epithelial cell lining leading to cell death

  •  a local inflammatory response would be activated– part of the inflammatory response includes neutrophil infiltration which explains the presence of neutrophils and patient stool samples

  •  spontaneous cure / self-limiting disease progression may occur within 2 to 7 days

  •  patients may succumb to the disease if not well-managed– especially in infants and elderly 

  1. Enter epithelial cell in intestinal tract

  2. Multiply inside cell (where safe from immune response)

  3. Invade neighboring epithelial cells and evades immune defense (can proceed to inc distance across entire intestinal tract)

  4. An abscess forms (cells falls apart) as epithelial cells are killed by the infection

    1. The bac rarely spread into the blood stream

    2. Since intracellular travel is not needed, can evade immune cells like neutrophils

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S. Aureus: mechanism of poisoning

  • when symps appear and 3 symps

is ingestion of food contaminated during preparation or storage

  1.  bacteria grow and release enterotoxin into food, doing all the damage like with toxic shock syndrome

  2.  toxin is performed when ingested

  3.  symptoms appear to 8 hours after ingestion (some bac but lots of toxin); GI symptoms of vomiting and diarrhea, headache typically 

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Salmonella: invasiveness, intracellular viability, toxins (2)

  • Invasiveness

    • Like shigella, invades the epithelial lining but does not reside in the epithelial lining and instead penetrates (goes through) the epithelial lining into subepithelial tissue

  • Intracellular viability

    • After invasion, the bac are ingested by macrophages where they multiply and pass to other body sites

    • The ability to survive intracellularly is due to specific surface O antigens or in the case of salmonella typhi, the presence of Vi (virulence) capsular antigen

      • S. typhi presence of Vi antigen makes more virulent than those without→Vi anti prevents intracellular destruction of the bac by phagocytic cells (protective virulence factor)

  • Endotoxins

    • Upon destruction of the salmonella, endotoxin (gram neg O antigen LPS) is released and responsible for fever and shock manifested during salmonella septicemia

  • enterotoxins 

    • Have cytotoxic (cell killing) and enterotoxic (intestinal poisoning) properties

    • Patients infected with salmonella strains producing enterotoxin have inc fluid loss and inc inflam components

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Incubation period

Shigella–

S. aureus–

Salmonella–

Shigella–2-3 days

S. aureus–symptoms appear to 2-8 hours after ingestion (some bac but lots of toxin);

Salmonella– 18 hrs

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Fever?

Shigella–

S. aureus–

Salmonella–

Shigella–fever

S. aureus–no fever

Salmonella–fever

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Symptoms

Shigella–

S. aureus–

Salmonella–

  • what is usually present in addition in salmonela (in terms of WBC)

Symptoms

Shigella– appear abruptly, fever, abdominal pain, cramps, bloody diarrhea with mucus, usually neutrophils (WBC response)-->serious concern and occurs last in progression; electrolyte imbalance and dehydration can be life threatening

S. aureus–GI symptoms of vomiting and diarrhea, headache typically 

Salmonella–Is an acute infection with continuous fever, skin eruptions, bowel disturbances, toxemia (toxic prod in blood) 

  • Leukopenia (dec WBC) is usually present

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Name the most common species of Shigella isolated in the United States.

S. sonnei (D)- Sonne-Duval bacillus =>60-80% of shigella reported in US

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Causative agent

Bac dys:

Typhoid fever: (one primarily to man and one for animals)

  • how spread

Bac dys: all shigella species

Typhoid fever: salmonella that primarily affects man (human is only natural host/carrier of)=S. Typhi (salmonella enteritidis ssp typhimurium)

  • Common to man but limited patho in animals

  • Salmonella that primarily affects lower animals but CAN prod disease in man= S. enterica ssp enterica

  • Presence of salmonella in habitats other than the natural hosts (water, food, natural env) is explained by presence of fecal contam from infected animals

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Determinants of pathogenicity bac dysentry vs thyphoid fever

  • toxins (1 for bac dys 2 for salmo)

  • relation to epithelial cell invasion

Bac dys: Shigella is an invasive bacteria that enters a small intestine where it multiplies

  • it then proceeds to the mucus surface of the terminal ileum and colon

  •  bacteria multiply in the epithelial cells

  •  it invades the epithelial cells where it resides and causes abscess formation and sloughing of epithelial cell lining leading to cell death

  •  a local inflammatory response would be activated– part of the inflammatory response includes neutrophil infiltration which explains the presence of neutrophils and patient stool samples

  •  spontaneous cure / self-limiting disease progression may occur within 2 to 7 days

  •  patients may succumb to the disease if not well-managed– especially in infants and elderly 

  • shiga toxin that is type of enterotoxin with cytotoxic effects

Summary: 

  1. Enter epithelial cell in intestinal tract

  2. Multiply inside cell (where safe from immune response)

  3. Invade neighboring epithelial cells and evades immune defense (can proceed to inc distance across entire intestinal tract)

  4. An abscess forms (cells falls apart) as epithelial cells are killed by the infection

  1. The bac rarely spread into the blood stream

  2. Since intracellular travel is not needed, can evade immune cells like neutrophils

Typhoid fever/salmonella:

  • Invasiveness

    • Like shigella, invades the epithelial lining but does not reside in the epithelial lining and instead penetrates (goes through) the epithelial lining into subepithelial tissue

  • Intracellular viability

    • After invasion, the bac are ingested by macrophages where they multiply and pass to other body sites

    • The ability to survive intracellularly is due to specific surface O antigens or in the case of salmonella typhi, the presence of Vi (virulence) capsular antigen

      • S. typhi presence of Vi antigen makes more virulent than those without→Vi anti prevents intracellular destruction of the bac by phagocytic cells (protective virulence factor)

  • Endotoxins

    • Upon destruction of the salmonella, endotoxin (gram neg O antigen LPS) is released and responsible for fever and shock manifested during salmonella septicemia

  • enterotoxins 

    • Have cytotoxic (cell killing) and enterotoxic (intestinal poisoning) properties

    • Patients infected with salmonella strains producing enterotoxin have inc fluid loss and inc inflam components

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Source (reservoir)

Bac dys:

Typhoid fever/salmonella: (man/animal)

Source (reservoir)

Bac dys: humans

Typhoid fever/salmonella: man→s. typhi/animal→s. Enterica fecal contam of water, food, env

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Method of transmission

Bac dys:

Typhoid fever/salmonella: (risk group)

bac dys: human to human 

  • Reservoirs are human carriers who shed the bac in their feces

  • Spread via flies, fingers, food, and water

Typhoid fever/salmonella: ingestion of fecally contam food/water

  • Anyone can get–greatest risk is for travelers visiting countries where the disease is common

  • Chronic carrier state exists for salmonella infect

  • Infected host may have disease (+symp)

  • May have infection but be asymptomatic

  • May be chronic carrier: carrier stage varies from days to years; 3% of cases become lifelong carriers

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Best patient specimen to use for testing

Bac dys:

Typhoid fever/salmonella:

Lab diag:(1—2 places and when to get specimin)

Sero typing: epidemiology studies (2)

Bac dys: rectal swab of an ulcer taken by sigmoidoscopic examination (similar to colonoscopy)

Typhoid fever/salmonella:

Lab diag:

  • Biochemical tests

  • Isolation of salmonella constitutes pos lab diag of salmonellosis

  • Serological typing may be done to det. Specific strain (sometimes prob in community and want to know commonality)

  • Appropriate specimen for lab testing dep on stage bc as salmonella dec in blood, goes to inc in stool samples; specimen of greatest interest is where symp appear

    • If having diarrhea, stool samp (during acute stages of gastroenteritis)

    • If having fever, blood culture (during septicemia and enteric fevers)

Sero typing: epidemiology studies

  • Kauffman-White: based on surface antigens

    • Gives species statues to each antigenic type

    • Many diff antigenic types (1500-200) based on O and H antigens 

    • Bc number of possible serotypes possible, only large reference centers are capable of typing salmonella isolates

  • Ewing: used by CDC–3 species of genus salmonella

    • S. typhi

    • S. cholerae-suis

    • S. enteritidis

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Clinical infection

Bac dys vs Typhoid fever/salmonella

WBC/bloodstream effects of each

Bac dys: appear abruptly, fever, abdominal pain, cramps, bloody diarrhea with mucus, usually neutrophils (WBC response)-->serious concern and occurs last in progression; electrolyte imbalance and dehydration can be life threatening

Typhoid fever/salmonella: 

  • Is an acute infection with continuous fever, skin eruptions, bowel disturbances, toxemia (toxic prod in blood) 

  • Leukopenia (dec WBC) is usually present

    • Probs due to depression of white blood cell maturation in the bone marrow and or early release from the bone marrow because of S. typhi

    • Increase incidents of immature white blood cell and bloodstream leads to inc incidents of immature white blood cell in the blood stream→to not functional/ as functional phagocytosis 

WEEK 1  ENTERIC FEVER manifestations: constipation>diarrhea is the rule

  • During this time, the salmonella are penetrating the intestinal wall, infecting the lymphatic system, multiplying intracellularly in host cells, being carried to the mononuclear phagocyte system (MPS: formerly known as RES) by the bloodstream where phagocytosis occurs in the lymphatics and MPS

WEEK 2: when symp really start manifesting

  • Bac re-enter the bloodstream, bacteremia dev, bac lyse, endotoxin released, patient becomes severely ill

    • Fever of 104 deg F (40 deg C)

    • Delirious

    • Abdomen is tender

    • Abdomen has rose colored spots that appear (*unique symp that look for ID and begin to look for how to tret)

  • Salmonella then reinfects the intestinal tract

    • Diarrhea

    • Necrosis (cell death that is so fast, accumulates bc don’t have enough time to remove by normal mech) and sloughing of intestinal lining

    • Intestinal ulceration develops (open wounds/sores)

    WEEK 3: 

    • Patient remains febrile

    • Patient shows improvement if no complications develop (often do)

    COMPLICATIONS: Most deaths associated with typhoid fever are due to complications

    •  severe bleeding due to necrosis of blood vessels during the ulceration process

    •  perforation of intestinal wall due to extensive ulceration

    •   Cholecystitis 

      •  inflammation of the gallbladder due to presence of salmonella

      •  bacteria may be found in the gallbladder years later

    IMMUNITY: And 90% of the cases, resolution of an attack of typhoid fever provides the patient with lifelong immunity

    •  Serologic diag and graph is useful because can ID when patient is an infection course

    •  

      • In week one there is a large amount of antibodies in the blood culture and low amount in stool and urine samples

      • Bacteria in blood stream→ decrease antibodies in blood, increase antibodies in stool and urine→ increase antibodies in serum, all other categories go down (stool and urine)→ body recovers from infection because of antibody presence

        • When antibodies begin to decrease we know that patient has recovered because they are no longer needed to fight the infection

        •  if there are no antibodies / no antibodies decreasing patient might be chronic carrier 

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salmonella vaccines—2, % effective and agaimst what infection specifically

  • No salmonella vaccine used in humans is 100% effective, but 2 typhoid vaccines available in the US

    • Ty21a sold as Vivotif Berna: made by swiss serum and vaccine institute

    • ViCPS sold as Typhim Vi: made by pasteur merieux 

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Treatment

Bac dys: 3

Typhoid fever/salmonella: 

Uncomplicated gastroenteritis:

Enteric fever or septicemia: (2—sus testing why)

  • major threats to complications

Bac dys: Since disease is self-limiting, frequently no treatment is sought

  •  ampicillin, tetracycline, chloramphenicol

  • Fluid and electrolyte balance may be needed depending on severity of disease

Typhoid fever/salmonella: Usually self-limiting (lasts 2-5 days)

  • Complications: dehydration, electrolyte imbalance are major threats

Uncomplicated gastroenteritis:

  • Self limiting, manage fluid and electrolyte balance

  • Antibiotic therapy may prolong the carrier state and help promote rez strains

Enteric fever or septicemia: 

  • Ampicillin or chloramphenicol are drugs of choice

  • Sus testing needed to ID rez strains

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Prevention

Bac dys:

Typhoid fever/salmonella:

Prevention

Bac dys: Sanitation consists of proper sewage disposal, water purification/chlorination, identification and treatment of carriers, carriers should not be allowed to handle food (no restaurant work or food processing)

Typhoid fever/salmonella: No salmonella vaccine used in humans is 100% effective, but 2 typhoid vaccines available in the US

  • Ty21a sold as Vivotif Berna: made by swiss serum and vaccine institute

  • ViCPS sold as Typhim Vi: made by pasteur merieux 

Prevention/control:

  • Detection and treatment of carriers–esp those w/ S.typhi

  • Control of transmission

  • Sanitation

  • Proper handling of food (refrigeration and proper cooking)

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Describe “carrier state” relevant to a disease. Identify an organism that can produce the carrier state. Discuss the importance of carrier states.

  • In 1907, Mary Mallon, aka Typhoid Mary, became the first American carrier to be identified– before her, didn't realize concept of carrier who can have infection with no symptoms 

  • Mallon’s employment history was traced back to 1900s and was identified that typhoid breakouts followed her from job to job→ knew that she was the link, didn't know how

  •  from 1900 to 1907 (no handwashing regularly)Mary worked at seven jobs in which 22 people became ill with typhoid fever, including one girl who died shortly after she came to work for them as a cook

  •  Mary resisted accusations that she was the cause of people getting sick and dying and stated that she never had typhoid

  •  finally she consented to a test for typhoid and typhoid bacilli was done for stool samples

  •  typhoid/salmonella is not the only infection with a carrier component

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Discuss the different classification schemes of Salmonella based on serologic typing. Name the scheme used and the 3 species identified by the Centers for Disease Control and Prevention.

  • Ewing: used by CDC–3 species of genus salmonella

    • S. typhi

    • S. cholerae-suis

    • S. enteritidis

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  1. Name (genus, species) the predominant facultative microbe in the intestine.

         2.     Describe the morphology of Enterobacteriaceae when Gram stained.

         3.     Classify E. coli on the basis of lactose fermentation.

         4.     Describe mechanisms by which E. coli may cause diarrhea.

  1. Escherichia coli

         2.     Gram neg rod

         3.     If pathogenic strain, lactose neg 

         4.     Enterotoxins–specific toxin for cells of intestinal mucosa that cause GI upset

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travelers dirrhea type

shiga-like toxin prod

infantile and childhood diherhea

enterotoxin

of these choices: ETEC, EPEC, EHEC

ETEC

EHEC

EPEC

ETEC

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Name the pathogenic E. coli and describe their pathogenic effects.

EHEC (___)-->EHEC ____

EPEC (____)

ETEC (____)

EIEC (_____)

EaggEc (_____)→ primary cause of ___in ____ patients

EHEC (enterohemorrhagic)-->EHEC O157:O7

EPEC (enteropathogenic)

ETEC (enterotoxigenic)

EIEC (enteroinvasive)

EaggEc (enteroaggregative)→ primary cause of chronic diarrhea in HIV patients

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Describe and discuss Shiga toxin; include organisms from which it is found, pathologic states it causes.

  • occurs in ___% patients with what strain of E. coili and results in what % death and % renal disease

  • implicated food prods

  • toxin damages what, how

  • lab ID (3)

Shiga-toxin producing E. coli O157:H7 (EHEC): 

  • Important pathogen in North America

  •  produces Shiga toxin (exotoxin) which is the same toxin as in produced by shigella dysenteriae hence the name

  •  most important disease complications of E coli 0157:H7 is development of hemolytic uremic syndrome (HUS)

    •  occurs in 5 to 10% of patients with the strain and results in 5% death or 30% chronic renal disease 

  • Infection is transmitted primarily by food, water, direct contact with bacteria like swimming in contaminated water

  •  implicated food products are ground beef, salami, raw milk, Alfalfa sprouts, unpasteurized apple cider and apple juice, contaminated pork, poultry, lamb, bagged fresh spinach

  • toxin damages capillary lining→ platelets clump in the area to stop blood loss and initiate healing →platelets form mesh and capillaries causing damage to RBCs which prevents adequate blood flow to affected organs→ results in organ dysfunction or failure due to 85% occlusion of blood vessel 

  • Lab ID is easily performed with specialized media, PCR (for fast turnaround time), agglutination reactions (that are antibody-antigen assays), enzyme linked immunosorbent assay (ELISA) testing stool culture→ using antibody against toxin specifically to ID antigen in stool specimen

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Describe the term “self-limiting” as related to clinical course of infection.

Will resolve on own–no antibiotics needed to resolve infection

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State the common name for Klebsiella pneumoniae.

Friedlander’s bacillus

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Tribe: klebsielleae

3 types, opportunistic or obligate

leading cause of ___infections

cost commonly isolated member of tribe

3 Predisposing cond

symos

why speutum with blood

  • Bac in genre are opportunistic pathogens

  • Klebsiella

  • Enterobacter

  • Serratia

  • Some of these bac have become leading cause of hospital acquired infections in US

  • Most commonly isolated member of the tribe is Klebsiella pneumoniae

    • Casuitive agent of pneumonia

    • Also causes infection at other body sites

    • 2nd most populous enteric genus found in the intestine of man that is a constituent of the normal intestinal flora (Escherichia ranks 1st–E. coli)

Clinical infection of pneumonia (K. pneumo):

  • K. pneumoniae causes primary pneumonia

    • Common patients affected are those in debilitated states

    • Predisposing cond exist: alcoholism, chronic obstructive pulmonary disease (COPD), diabetes mellitis

  • Seriousness of infection is realized by its high mortality rate (~50% despite treatment w/ appropriate antimicrobics)

  • Symp: chest pain, fever, shaking, chills, shortness of breath (not enough room in lungs for breath)

  • Coughing up sputum containing blood is an indication of serious infection→vasculature supplying blood to lungs are bleeding

  • Symps indicating a med emergency include: high fever, rapid HR, low BP, blue-grey pallor indicative of poor tissue oxygenation, mental confusion/delirium from high fever

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Other infections K. pneumo: (other than pneumo)—5, and why one is same for all enterics

  • Abscess formation (bleeding in sputum) and tissue necrosis of the bronchi occur more often with Klebsiella pneumo more than w other bac pneumonia

  • Besides primary pneumo, K. pneumo has been opportunistically associated w/ UTI (all enterics bc close prox to stool tract), wound infections, septicemia, meningitis

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Treatment K. pneumo:

  • what is Klebsiella usually rez to (2)

  • why might sus be needed

  • Antimicrobics are warranted in klebsiella infections

  • Sensitivity testing needs to be performed to assure appropriate antimic regime indicated (may be ESBL/ extended spec beta-lactamase bac or other emerging microbe of concern)

    • Not evident if EBSL so must do special testing

    • Klebsiella pneumo is usually resistant to ampicillin and carbenicillin (via R-factor plasmids)

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Classify Klebsiella pneumoniae on the basis of lactose fermentation.

Since normal flora of intestinal tract, lactose pos

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Relate predisposing debilitating factors to a primary pneumonia caused by Klebsiella.—3

  • mortality rate

  • K. pneumoniae causes primary pneumonia

    • Common patients affected are those in debilitated states

    • Predisposing cond exist: alcoholism, chronic obstructive pulmonary disease (COPD), diabetes mellitis

  • Seriousness of infection is realized by its high mortality rate (~50% despite treatment w/ appropriate antimicrobics)

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Name the enteric organism that produces a red pigment

S. marcescens  

  • Red pigment on plated agar media (no other organism w similar pigment)

  • In pneumo infection, Cough up red sputum that is not blood but often mistaken as blood

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proteeae 3 genre of importance

  1. Proteus

    1. P. vulgaris

    2. P. mirabilis

  2. Providencia

    1. P. alcalifaciens

    2. P. stuartii

    3. P. rettgeri

  3. Morganella

    1. M. morganii

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Clinical infections and Lab diag proteeae tribe

  • opportunistic or obligate path

  • extraintestinal disease states (4—main one and relation to E.coli)

  • what is unique ab lab diag on plate

  • lactose ___

Clinical infections

  • Constitute normal flora of the intestinal tract

  • Since proteeae tribe of bac are lactose neg normally (when nonpathogenic), so complete evaluative assessment of these bac in feces samples is necessary 

    • Need to be ruled out as pathogenic bac *exception to rule of lac neg being intestinal pathogens

  • Like other opportunistic enterobacteriaceae, they cause infections at other body sites

  • Extraintestinal disease states include:

    • UTI (members of Proteus genus rank 2nd to E.  coli as most common causative agents of UTI)

    • Wound infections

    • Pneumonia

    • Septicemia 

Lab diag proteeae tribe

  • Biochemical testing

  • Actively motile (swarm)

  • Are lactose neg

    • Must be diff from enteric pathogens when culturing stool samples

    • Can conceal other bac in mixed growth plate so need to isolate out pathogens if multiple

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State the major type of infections caused by Serratia marcescens.

  • why now ___pathogen (opp or obl)—>story from 1950

  • known to cause 5 infections—>what is main link between them

Serratia genus

  • Were considered harmless/nonpathogenic and were used to det germicidal efficacy and air current flow in hospitals (all organisms are opportunistic, we may not have recog disease yet)

S. marcescens 

  • In 1950, army used a ship to conduct exp bio attack in san fran bay (op sea spray)--> spread cloud of S. marcescens for purpose of studying offensive possibilities of attacking sea port city with aerosol biowarefare from offshore

    • Few days later, 11 residents were admin to hosp w/ S. marcescens infect that has never been seen before

    • In 1969, S. marcescens was recog as a bac marker for studying dissemination of bac aerosols was disct.

  • are now recog as an opportunistic pathogen associated w/ predisposing factors:

    • Underlying diseases (primary disease present which can lead to secondary disease due to serratia)

    • Immunosuppressive treatment (HIV/AIDS patients, organ transplant recipients, chemotherapy)

      • More pop now

  • Known to cause infections of the endocardium, blood, wounds, UTI, resp tract

  • Has emerged as a major cause of hospital acquired (nosocomial) infect

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Clinical infection (hosp acquired) S. marcescens:

  • 5

Treatment of infect of S. marcescens: how sus/rez is it

Lab diag S. marcescens:

  • what testing

  • unique quality on plate

Clinical infection (hosp acquired) S. marcescens:

  • Pneumo

    • Sometimes transmitted by contaminated equipment used for resp care treatments (now all disposible)

  • Spetecemia

  • Meningitis

  • Wound infections

  • UTIs

    • Usually associated w/ underlying abnormalities (kidney disease, bladder retention)

    • instrumentation (contaminated catheter)

Treatment of infect of S. marcescens:

  • Known for their rez to a wide range of antimics

  • Sus tests must be performed on each isolate to det appropriate antimicrobial therapy 

Lab diag S. marcescens:

  • Biochem testing

  • Red pigment on plated agar media (no other organism w similar pigment)

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Describe what is meant by the term “swarming” when referring to a cultural characteristic. Name the bacteria that display the “swarming” characteristic.

Lab diag proteeae tribe

  • Biochemical testing

  • Actively motile (swarm)

  • Are lactose neg

    • Must be diff from enteric pathogens when culturing stool samples

    • Can conceal other bac in mixed growth plate so need to isolate out pathogens if multiple

  • "swarming" refers to the rapid, coordinated movement of a population of bacteria across a solid or semi-solid surface. It is a collective, multi-cellular behavior that enables bacteria to spread and colonize new territory faster than individual cells could. 

    • Results in concentric circles around a single center colony

<p><span style="background-color: transparent; font-family: &quot;Times New Roman&quot;, serif;">Lab diag <strong>proteeae tribe</strong></span></p><ul><li><p><span style="background-color: transparent; font-family: &quot;Times New Roman&quot;, serif;">Biochemical testing</span></p></li><li><p><span style="background-color: transparent; font-family: &quot;Times New Roman&quot;, serif;">Actively motile (swarm)</span></p></li><li><p><span style="background-color: transparent; font-family: &quot;Times New Roman&quot;, serif;">Are lactose neg</span></p><ul><li><p><span style="background-color: transparent; font-family: &quot;Times New Roman&quot;, serif;">Must be diff from enteric pathogens when culturing stool samples</span></p></li><li><p><span style="background-color: transparent; font-family: &quot;Times New Roman&quot;, serif;">Can conceal other bac in mixed growth plate so need to isolate out pathogens if multiple</span></p></li></ul></li></ul><p></p><ul><li><p><span style="background-color: transparent; font-family: &quot;Times New Roman&quot;, serif;">"swarming" refers to the rapid, coordinated movement of a population of bacteria across a solid or semi-solid surface. It is a collective, multi-cellular behavior that enables bacteria to spread and colonize new territory faster than individual cells could.&nbsp;</span></p><ul><li><p><span style="background-color: transparent; font-family: &quot;Times New Roman&quot;, serif;">Results in concentric circles around a single center colony</span></p></li></ul></li></ul><p></p>
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Edwardsielleae tribe

  • how common infections

  • The only recognized human pathogen in this tribe

  •  has been isolated from (4)

  • Edwardsiella tarda= The only recognized human pathogen in this tribe

  •  rare infections

  •  has been isolated from wound infections, gastroenteritis/inflammation of stomach and intestinal lining, sepsis, meningitis

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Enterobacter

  • 2 Clinically sig enterobacter specie

  • Both tend to be o____ pathogens

  • which associated w/ UTIs

  • isolated from what 3 locations

  • Clinically sig enterobacter species= E. cloacae, E. aerogenes

  • Both tend to be opportunistic pathogens

  • E. cloacae have been associated w/ UTIs

  • Both have been isolated from wounds, blood, spinal fluid

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3 most important species Yersinia

Y. entercolitica, pseudotuberculosis, pestis

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Lab ID Yersina (3)—gram stain morph, wayson stain morph, temp req for optimum growth

biochemical testing, lactose neg on MacConkey agar, Wayson stain

a.     Gram stain morphology: gram neg rod

b.     Wayson stain morphology: bipolar staining with Wayson stain with safety pin appearance

c.     Temperature requirement for optimum growth 4 deg C (refrigerator temp)

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Y. entercolitica

  • source

  • transmission

  • pathogenesis (invasion—body part and clinical cond)

  • occurs most freq in what age group

  • sensitive or rez to most antimic?

  • source= intestinal tracts of domestic and wild animals

  • transmission= fecal-oral route–usually due to food or water contam; occurs animal to person or person to person

  • Pathogenesis: 

    • Invasion: primarily causes intestinal infection, enters via the oral digestive route with infection in the terminal ilium (near appendix), adheres to and penetrates the ileum causing terminal ileitis, lymphadenitis, and acute enterocolitis 

    • Clinical cond following intestinal infection: erythema nodosum or other skin rashes, polyarthritis (arthritis that moves and presents in several joints), septicemia (less common)

  • Occurs most frequently in children 

  • Treatment: organism is sensitive to many antibi and usually self limiting (unless immunocomp like blood transfusion patients)

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lab diag Y. enterocolitica 

  • specimin best recovered from what samples incubates at what temp

  • test for ID

  • isolation how from other species

  • Specimen: organism is best recovered from stool samples that are incubated at room temp

  • Isolation: use of cold enrichment media enhances its isolation from patient samps (4 deg C is unique temp to grow at)

  • Biochem tests: for ID

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Briefly describe the symptoms associated with Y. enterocolitica infection in: infants, older children, adults

a.     Infants (<2) acute diarrhea, fever

b.     Older children (2-15) diarrhea though not as severe as infants, fever, abdominal pain, freq mimics appendicitis (primarily tenderness w/ touching abdom, feeling of intestinal upset, fever)

c.     Adults weak primary symptoms: slight fever, abdom pain, polyarthritis, rash lasting up to 4 mo

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Relate optimum growth temperature of Yersinia enterocolitica to medical importance for Blood Banks that distribute units of blood for use in patients.

  • what causes symps of shock and chills

  • Cases of contam units of blood have been reported (blood donor asymp, but since organism grows at 4 deg C, the temp blood is stored, bac multiply and can cause infection)

  • Most bac die or halt growth at this temp

  • When blood unit is infused into a recipient, transfusion reaction occurs with symps of chills and shock due to endotoxin

  • Medical symptoms of importance

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State the disease caused by Yersinia pestis.

Formerly known as Pasteurella pestis, classic species of genus Yersina, causative agent of the plague (black plague)

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1st, 2nd, 3rd, and current pandemics/epidemics/occurrences of plague (Y. pestis)

  • % pop died in second 2 pandemics

History of plague pandemics:

1st documented pandemic was 542 AD and lasted 60 years

2nd pandemic: “black death” in 14th C

  • Spread through asia, europe, china, india with high mortality

    • 25% of total pops of these countries 

  • European phase (1348-1350)

    • 44% of pop died (40 mil/90 mil)

3rd pandemic: started in 1855

  • Entire world was affected–including US

  • Wide reservoir of carriers was established (such as wild rodents like rats)

Current: 

  • Still exists endemically in africa, south america, asia, former USSR

  • Surge of cases in india (several 100 had, 50 died)-->due to inc pop of rats after monsoon floods

  • Sporadic cases in US usually result of contact w/ wild or domestic animals 

  • No cases of human to human transmission recorded since 1924

  • Recent epidemic in madagascar (place regularly outbreaks but less dangerous version)-->rats to humans by fleas

  • In US most incidences are in SW/ cali

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how is Y. pestis same from tribe (morpho, 2 stains, lactose) and how diff (media)

Same as tribe:

  • gram neg rods (coccobacilli)

  • Bipolar staining w/ wayson’s stain

  • Lactose neg

Diff from tribe members: grows on ordinary media at 37 deg C→cold enrichment media is not needed

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y. pestis immuity and antibi of choice

  • vaccination?

  • Survivors have life long immunity

  • treatment=antimic of choice is streptomycin

  • Vaccination is rec for lab and field personnel working w/ organism, researchers, peace corp volunteers working in regions where endemic

    • Not common disease in general pop so not widely used vaccine

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Explain the (2 which hinted below) mechanisms by which Y. pestis is transmitted to man, including the major source of the organism.

  • #s

  • hosts

  • Highly pathogenic for many animals: number of  bac req to initiate infection is small (3-50 bac cells)

  • Exists naturally in many animal hosts

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Transmission is a cycle of hosts: Y. pestis

3

  1. Reservoir hosts harbor organism but have no sign of disease–can be long term reservoirs (like for whole life)

  • Do not develop disease

  • Rodents like mice and voles

  • Spread bac to other mammals (amplifying hosts)

  1. Amplifying hosts become infected, have disease, die (massive die-offs is way to recog this stage)

  • Massive die offs occur during epidemics

  • Rats, ground squirrels, chipmunks, rabbits

  1. Accidental hosts become infected via amplifying hosts (humans)

  • Become infected by receipt of organism from flea bite, handling infected animals, animal skins, meat, or by inhaling droplets containing the bac

  • Transmission from long-term reservoirs to amplifying hosts to humans is mostly by fleas (bubonic with dev of lesions)

    • After an uninfected flea has a blood meal from a plague infected animal;. The plague bacilli multiply in the gut of the flea,

    • Subsequent blood meals for the flea contain regurgitated infectious material

  • Plague occurs in 200 diff species of mammals

  • Transmission to humans can also be by aerosol or septicemic movement to lungs (pneumonic)

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List the three forms of plague and identify the major clinical symptom for each.

  • mortality if each?

Bubonic:

  • Sudden, high fever

  • Headache

  • Chills

  • Body aches

  • Swollen, painful lymph nodes at the groin and armpits (buboes)

    • Organism filled swellings

    • Most common is femoral lymph node

    • Next most common is inguinal, axillary, cervical

    • Location of buboes is a function of the region of the body where an infected flea bit the person and inoculated plague bacilli into the bite

  • Organism enters skin through flea bite, is carried by lymphatic system to lymph nodes usually under the arms and in the groin

  • Organism multiplies, forms inflam abscesses in lymph nodes (buboes) which are extremely painful

    • Won’t kill patient in itself, usually only when progress to other stages

  • Classic clinical findings are fever, chills, malaise and regional buboes

  • Mortality is up to 50% if untreated (leads to septicemic plague)

    • Buboes freq drain into the bloodstream causing septicemia

Pneumonic:

  • Sudden pneumonia

  • Bloody, watery mucous

  • Resp failure

  • Occurs due to spread of bubonic or septicemic plague (vasculature in lungs) to lungs or direct involvement of the lungs via inhalation of droplets spread by an infected human

  • High mortality (up to 100% if untreated) that occurs rapidly (symp onset to death can be <2 days)

  • Highly contagious

  • Symps include CNS disorders such as convulsions, stupor, lack of coordination

Septecemic: 

  • Fever, chills, body aches, severe abdom pain

  • Shock

  • Blackened skin at the extremities due to necrosis of the body

  • Organism enters through flea bite, profound septicemia early in disease

  • Can result from bubo drainage into bloodstream, but can also occur w/ no bubo formation

  • Rapid vascular collapse peripherally

  • DIC

  • High mortality (up to 100% if untreated)

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Define the terms bubo, long term reservoirs and amplifying hosts and relate these terms to Yersinia pestis.

bubo= Swollen, painful lymph nodes at the groin and armpits 

  • Organism filled swellings

  • Most common is femoral lymph node

  • Next most common is inguinal, axillary, cervical

  • Location of buboes is a function of the region of the body where an infected flea bit the person and inoculated plague bacilli into the bite

Long term reservoir=hosts that harbor organism (plague/ Y. pestis) but have no sign of disease–can be long term reservoirs (like for whole life)

  • Do not develop disease

  • Rodents like mice and voles

  • Spread bac to other mammals (amplifying hosts)

Amplifying hosts=become infected, have disease, die (massive die-offs is way to recog this stage)

  • Massive die offs occur during epidemics

  • Rats, ground squirrels, chipmunks, rabbits

  • Accidental hosts become infected via amplifying hosts (humans)

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Explain why the name “Black Death” was given to the disease caused by Y. pestis.

Hemorrhaging occurs due to infection- induced DIC (disseminated IV coag) w/ resultant black splotches (septicemic plague) in the skin which caused the name black death to be given to the plague

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Describe the means by which pneumonic plague may be contracted.

  • Become infected by receipt of organism from flea bite, handling infected animals, animal skins, meat, or by inhaling droplets containing the bac

  • Transmission from long-term reservoirs to amplifying hosts to humans is mostly by fleas (bubonic with dev of lesions)

    • After an uninfected flea has a blood meal from a plague infected animal;. The plague bacilli multiply in the gut of the flea,

    • Subsequent blood meals for the flea contain regurgitated infectious material

  • Plague occurs in 200 diff species of mammals

  • Transmission to humans can also be by aerosol or septicemic movement to lungs (pneumonic)

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Explain why routine laboratories do not attempt to culture suspected cases of plague.

  • BSL category and requirements (3)

  • category of agent (A, B, or C)

Cultures Y. pestis

  • Immediately sent to labs w/ special facilities able to contain spread

  • Category A agent (easily transmitted, high mortality)

  • Req BSL-3 precautions (hosp are BSL 2, so need to contact public health dep and CDC for their labs)

    • BSL 3= level 2 + special clothing, controlled access, directional airflow

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collection of Y. pestis specimen of interest (3)

  • Depends on symptom displayed by indiv

    • Bubonic–bubo aspirate w/ needle and syringe to withdraw fluid

    • Septicemic–blood

    • Pneumonic–sputum, throat

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who expereinces K antigen interference

salmonella, shigella, yersina

shigella

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who experiences HUS as a complication

E. Coli 0157:H7

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exotoxin vs enterotoxin vs endotoxin

exo= shiga tox (gram pos or neg can make)

entero=Gi tox

endo= LPS gram neg tox —> shock

all enteric bac have these

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which bac species and genus is H2S pos in addition to lactose negative (no color on MacConkey agar)

salmonella

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what tribe needs to be ruled out as a pathogen because it is gram negative even though it is an enteric normal flora

proteeae

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cholecystitis?

inflam of gallbladder due to salmonella complication

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second most populous enteric genus (and most pop species from this genus) found in intestine as normal flora

klebsiella pneumoniae