Enterobacteriaceae II Flashcards

1
Q

Shigella

A
  • Gram -
  • bacilli
  • facultative anaerobe
  • Shigella is the classic cause of dysentery which is typically spread person-to-person under poor sanitary conditions.
  • The illness begins as a watery diarrhea but evolves into an intense colitis with frequent small volume stools containing blood and pus.
  • Despite the invasive properties of the organism the infection usually does not spread outside the intestinal tract.
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2
Q

Shigella Organism

A
  • Four species are defined by biochemical reactions and specific O antigens organized into serogroups
  • Shigella dysenteriae (serogroup A), Shigella flexneri (serogroup B), Shigella boydii (serogroup C), and Shigella sonnei (serogroup D).
  • All but S. sonnei are further subdivided into a total of 38 individual O antigen serotypes specified by numbers.
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3
Q

Shigellosis Epidemiology

A

Shigellosis is a strictly human disease with no animal reservoirs. Worldwide it is consistently one of the most common causes of infectious diarrhea in both developed and developing countries.

  • Readily transmitted by the fecal–oral route through person-to-person contact or by contamination of food or water.
  • Spread is efficient due to the low infecting dose shown to be less than 200 organisms.
  • Incidence of shigellosis is directly related to personal and community sanitary practices.
  • S. dysenteriae is largely limited to underdeveloped tropical areas.
  • S. dysenteriae, type 1 (Shiga bacillus) produces the most severe disease.
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4
Q

Shigellosis Pathogenesis

A
  • Shigella, is acid-resistant and survives passage through the stomach to reach the intestine. Once there the fundamental pathogenic event is invasion of the human colonic mucosa. This triggers an intense acute inflammatory response with mucosal ulceration and abscess formation.
  • Invasion and spread is a multistep process which is the same in Shigella and EIEC.
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5
Q

Shigellosis Invasion

A
  • Adhere selectively to M cells and can transcytose through them into the underlying collection of phagocytic cells
  • Inside M cells and phagocytic macrophages, the bacteria are able to cause their demise by activating normal programmed cell death (apoptosis).
  • Bacteria released from the M cell initiate a multi-step invasion process mediated by a set of invasin plasmid antigens (IpaA, IpaB, etc.). injected by an injection secretion system
  • Each Ipa has its individual action. These include cell attachment, cytoskeleton reorganization, actin polymerization, and induction of apoptosis.
  • Bacteria orient in parallel with the filaments of the cell’s actin cytoskeleton. Once attached thy initiate a process in which their control of the polymerization of actin fibrils to creates an actin “tail” behind the bacterial cell. This tail appears to drive the microbe through the cytoplasm like a comet.
  • When bacteria encounter the host cell membrane, they push it into the adjacent cell forming finger-like projections which eventually pinch off (like Listeria).
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6
Q

Consequences of Shigella Invasion

A

•This process creates focal ulcers in the mucosa particularly in the colon. The diarrhea created by this process is almost purely inflammatory consisting of small volume stools containing WBCs, RBCs, bacteria and little else.

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7
Q

Shigella and Stx

A
  • Some Shigella produce Stx which is not essential for disease but does contribute to the severity of the illness.
  • The most potent producer of Stx, S. dysenteriae type 1, is the only Shigella with a high mortality rate.
  • Disease severity is due to systemic effects of the toxin which can be the same as described for the EHEC including HUS.
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8
Q

Shigellosis Manifestations

A

•Shigella organisms cause an acute inflammatory colitis and bloody diarrhea, which in the most characteristic state presents as a febrile dysentery syndrome—a clinical triad consisting of cramps, painful straining to pass stools (tenesmus), and a frequent, small-volume, bloody, mucoid discharge

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9
Q

Shigellosis Diagnosis

A

•Shigella is readily isolated using selective media (such as Hektoen agar) which are part of the routine stool culture in clinical laboratories.

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10
Q

Shigellosis Treatment

A

•Because the disease is usually self-limiting, the beneficial effect of treatment is in shortening the illness and the period of excretion of organisms. Resistance rates to ampicillin, once the treatment of choice, have caused a shift to other antimicrobial agents.

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11
Q

Shigellosis Prevention

A

•Standard sanitation practices such as sewage disposal and water chlorination are important in preventing the spread of shigellosis.

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12
Q

Salmonella

A

Under a single species name, Salmonella enterica, the genus has been divided into hundreds of serotypes based on antigenic differences in O, K, and H antigens. The major groupings are:

  • Salmonella serotypes highly adapted to humans. The prototype is S. enterica serotype Typhi (hereafter S. Typhi), the typhoid bacillus
  • Salmonella highly adapted to animals.
  • Salmonella with a broad host range infecting humans and animals. Most Salmonella belong to this category and the bulk of human disease is caused by ten serotypes.
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13
Q

Salmonella Gastroenteritis – Salmonella enterica

A
  • The typical example of Salmonella “food poisoning” is the community picnic or bazaar, where volunteers prepare poultry, salads, and other potential culture media to be eaten later in the day.
  • Because the refrigerators are filled with beer and soda, the food is left out in covered pans. A near physiologic incubation temperature is provided by the still-warm contents and the afternoon sun. This allows the organisms to enter logarithmic growth during the softball game. The bacteria usually produce no noticeable change in the food.
  • One to two days after the feast, a significant portion of the revelers develop abdominal pain, nausea, vomiting, and diarrhea lasting for 3 or 4 days. An investigation points to a particular food such as potato salad or turkey dressing, which is found to have a correlation with both attack rate and severity of illness.
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14
Q

Salmonella Gastroenteritis Epidemiology

A

S. enterica gastroenteritis is predominantly a disease of industrialized societies and improper food handling which allows the transmission from the animal reservoir to humans.

  • Infecting dose is much higher than with Shigella; ingestion of 10,000 or more Salmonella bacilli is required.
  • Poultry products, are most often implicated as the vehicle of infection.
  • Raw milk and exotic pets such as turtles have been associated with outbreaks.
  • Multistate outbreaks of salmonellosis take place through the contamination of foodstuffs during large-scale industrial production.
  • Chronic carriers who are food handlers are an important reservoir.
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15
Q

Salmonella Gastroenteritis Pathogenesis

A

In Salmonella gastroenteritis the bacteria invade the enterocytes of the large and small bowel, transcytose through the basolateral membrane to enter the lamina propria, and induce a profound inflammatory response. Upon initial contact of bacteria with the intestinal brush border the normal architecture is dramatically altered within minutes.

• Surface adhesin(s) react with a host cell receptor to stimulate localized filamentous actin cytoskeletal rearrangement (membrane ruffling)

Bacteria are internalized by induced pinocytosis associated with ruffles.

• Injection (type III) secretion systems inject multiple effector proteins into host cells

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16
Q

Enteric Fever – S. Typhi

A
  • Typhoid fever has a slow, insidious onset and if untreated, lasts for weeks.
  • It ends either by a gradual resolution or in death due to complications like rupture of the intestine or spleen. The family notes only the extended fever although a physician may observe a subtle rash or feel an enlarged spleen. Diarrhea may occur once or twice during the course but is not a consistent feature.
17
Q

Enteric Fever – S. Typhi Epidemiology

A
  • Typhoid is a strictly human disease for which the primary reservoir is chronic carriers of S. Typhi.
  • Transmission is by the fecal-oral route when carriers contaminate food or water.
  • Infecting dose is intermediate between Shigella and most S. enterica and is lowered by the presence of the capsular Vi antigen which interferes with complement deposition in a manner similar to other bacterial capsular polysaccharides.
  • The decline in disease in industrialized nations largely reflects improved disposal of human waste.
18
Q

Enteric Fever – S. Typhi Pathogenesis

A

Following ingestion, the bacteria reach the small intestine where they traverse the mucosa to become ingested by macrophages. Rather than being killed by these phagocytic cells, the bacteria proliferate, and are carried through the lymphatic circulation to the mesenteric nodes, spleen, liver and bone marrow.

  • S. Typhi continues to multiply and the bacteria begin to enter the bloodstream.
  • Seeding of LPS endotoxin starts the fever, which rises and persists with the continuing bacteremia.
  • The bacteremia can also lead to the infection of the urinary tract and the biliary tree which causes reinfection of the bowel.
  • This cycle takes roughly two weeks to complete.
19
Q

Enteric Fever – S. Typhi Cellular Events

A
  • Bacteria bind to intestinal M cells and deliver the invading bacterium into the Peyer’s patch
  • S. Typhi invades macrophages where it multiplies within a membrane-bound vacuole that fails to fuse with other host-cell organelles. This leads to macrophage death.
  • Intracellular survival in professional phagocytes is due to inhibition of the oxidative metabolic burst.
20
Q

Shigella vs. Salmonella serotype Typhi

A
21
Q

Enteric Fever – S. Typhi Immunity

A

•The immune response to enteric fever is both humoral and cell mediated. In nonfatal cases, humoral antibody and activated macrophages will eventually subdue the untreated infection over a period of about 3 weeks.

22
Q

Salmonellosis - Gastroenteritis Manifestations

A
  • Begins 24 to 48 hours after ingestion, with nausea, vomiting, abdominal cramps and diarrhea.
  • Diarrhea persists for 3 to 7 days.
  • Fever is present in about half the patients.
23
Q

Salmonellosis - Bacteremia Manifestations

A
  • Frank sepsis may be seen in those with a compromised cell-mediated immune system.
  • Salmonella infection of the bone typically involves the long bones and sites of trauma, and sickle-cell injury
24
Q

Salmonellosis - Enteric Fever

A

Enteric fever is a multiorgan-system infection typically with S. Typhi characterized by prolonged fever, sustained bacteremia, and profound involvement of the reticuloendothelial system, particularly the mesenteric lymph nodes, liver, and spleen. In untreated patients the elevated temperature persists for weeks. Many patients are constipated, although perhaps one third of patients will have a mild diarrhea.

  • Chronic seeding of the bloodstream produces endotoxemia.
  • Persistent bacteremia leads to infection at other sites.
  • Biliary tree infection causes reinfection of the intestinal tract and diarrhea late in the disease.
  • Urinary tract, bone, joint, liver and meningeal infection may also occur.
  • The most important complication is hemorrhage from perforations through the wall of the terminal ileum at the site of necrotic Peyer’s patches.
25
Q

Salmonellosis Diagnosis

A

•Culture of Salmonella from the blood or feces is the primary diagnostic method. The media used for stool culture are the same as those used for Shigella. Early in the course of enteric fever the blood is far more likely to give a positive culture result than culture from any other site.

26
Q

Salmonellosis - Gastroenteritis Treatment

A

•The primary therapeutic approach to Salmonella gastroenteritis is fluid and electrolyte replacement and the control of nausea and vomiting. Antibiotic therapy is usually not used because it has a tendency to increase the duration and frequency of the carrier state. In patients with underlying risk factors, antimicrobial therapy is applied as a prophylactic measure aimed at preventing systemic spread.

27
Q

Salmonellosis - Enteric Fever

A

•Ampicillin and trimethoprim-sulfonamide have been the mainstays of treatment. Newer cephalosporins (ceftriaxone) and quinolones (ciprofloxacin) are effective against resistant strains.

28
Q

Klebsiella

A
  • The most distinctive bacteriologic feature of the genus Klebsiella is presence of a polysaccharide capsule.
  • K. pneumoniae, the most common species, is able to cause classic lobar pneumonia, a characteristic of other encapsulated bacteria.
29
Q

Enterobacter

A

Appears to be less virulent than Klebsiella

  • Usually found in mixed infections,
  • Hospital outbreaks traced to contaminated parenteral fluid solutions have implicated Enterobacter species.
30
Q

Proteus

A
  • Produces urinary tract and opportunistic infections
  • Production of potent urease enzyme contributes to formation of urinary stones. It is also useful for rapid laboratory identification.
31
Q

Yersinia

A
  • Includes Y. pestis, the cause of plague, which is covered with the bacterial zoonoses.
  • Both Y enterocolitica and Y pseudotuberculosis cause acute mesenteric lymphadenitis, a syndrome involving fever and abdominal pain that often mimics acute appendicitis. Y enterocolitica also produces a wider variety of manifestations. The most common of these is an enterocolitis, which usually occurs in children.
  • Wild animals are the reservoir for Y. pseudotuberculosis. Animals are also a source for Y. enterocolitica but the epidemiology is less certain.