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Gastrointestinal > Intestinal Infections > Flashcards

Intestinal Infections Flashcards

1
Q

What types of damage can be caused by gastrointestinal pathogens?

A
  • Local inflammation
  • Ulceration / perforation of mucosal epithelium
  • Disruption of normal microbiota
  • Pharmacological action of bacterial toxins
  • Invasion to blood or lymphatics
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2
Q

Describe the consequences of GI epithelial perforation.

A
  • Ruptured ulcer / perforated ulcer.
  • Lining of the mucosa wall is perforated due to untreated ulcers.
  • May result in leaking of food and gastric juices to the peritoneal or abdominal cavities.
  • Treatment requires surgery.
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3
Q

What are the incubation periods for the pathogens which cause diarrhoea, specifically campylobacter and shigella?

A
  • Campylobacter - 2-11 days
  • Shigella - 1-4 days
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4
Q

What are the durations of diarrhoea caused by campylobacter and shigella?

A
  • Campylobacter - up to 3 weeks
  • Shigella - 2-3 days
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5
Q

Describe the variable symptoms caused by the pathogens which cause diarrhoea, specifically campylobacter, shigella, EPEC and cholera.

A
  • Campylobacter and shigella - bloody stools.
  • EPEC and cholera - watery stools.
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6
Q

Describe the characteristics of vibrio cholerae.

A
  • Gram negative
  • Comma-shaped rod
  • Flagellated
  • Characterised by epidemics and pandemics
  • Human-only pathogen
  • Flourishes in communities with no clean drinking water / sewage disposal
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7
Q

What are the available vaccines for V. Cholerae?

A
  • Parenteral vaccine: low protective efficiency.
  • Oral vaccine: effective and suitable for travellers.
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8
Q

Describe the pathogenesis of V. cholerae.

A
  • Only infective in large doses.
  • Many organisms killed in the stomach.
  • Colonisation of small intestine involving flagellar motion, mucinase, attachment to specific receptors.
  • Production of multicomponent toxin.
  • Loss of fluid and electrolytes without damage to enterocytes.
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9
Q

Describe the characteristics of the cholera toxin (CTx).

A
  • Oligomeric complex of 6 protein subunits:
    • 1 copy of A subunit (enzymatic)
    • 5 copies of B subunit (receptor binding)
  • Responsible for the characteristic, watery cholera diarrhoea.
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10
Q

Describe the consequences of being infected by cholera.

A
  • Fluid loss of up to 1L per hour.
  • Electrolyte imbalance leading to dehydration, metabolic acidosis and hypokalaemia.
  • Hypovolaemic shock.
  • 40-60% mortality.
  • <1% mortality if given fluid / electrolytes (ORT).
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11
Q

Describe the characteristics of Escherichia coli.

A
  • Gram negative.
  • Bacillus.
  • Member of normal GI microbiota.
  • Some strains possess virulence factors enabling them to cause disease.
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12
Q

What are the types of E. coli which cause GI infections?

A
  • EPEC - enteropathogenic
  • ETEC - enterotoxigenic
  • VTEC / STEC - verocytotoxin-producing
  • EHEC - enterohaemorrhagic
  • EIEC - enteroinvasive
  • EAEC - enteroaggregative
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13
Q

Describe the different GI infections caused by the different types of E. coli.

A
  • EPEC: sporadic cases and outbreaks of infection in under 5s.
  • ETEC: ‘travellers’ diarrhoea’ (occurs in 20-50% of travellers).
  • VTEC / EHEC: sporadic cases and outbreaks of gastroenteritis.
  • EIEC: food-borne infection in areas of poor hygiene (often persistent diarrhoea).
  • EAEC: resource-poor countries.
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14
Q

Describe the factors which aid the adherence of E. coli.

A
  • Pili / fimbriae are used to attach the bacteria onto enterocytes.
  • Pedestal formation - this happens normally even in the absence of infection.
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15
Q

Describe the mode of action of E. coli enterotoxins.

A
  • LT = heat-labile toxin
  • STa = heat-stable toxin
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16
Q

Describe the characteristics of campylobacter jejuni.

A
  • Gram negative.
  • Helical bacillus.
  • Large animal reservoir.
  • Causes food-associated diarrhoea.
  • Commonest cause of diarrhoea in the developed world.
  • Transmission through comsumption of raw / undercooked meat, contaminated milk.
  • Mucosal inflammation and fluid secretion.
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17
Q

Describe the histological appearance of C. jejuni infection.

A
  • Inflammation involves entire mucosa.
  • Villous atrophy.
  • Necrotic debris in crypts.
  • Thickening of basement membrane.
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18
Q

Describe the characteristics of Salmonella spp.

A
  • Gram negative.
  • Bacilli.
  • >2000 serotypes of Salmonella spp.
  • Causes food-associated diarrhoea.
  • Transmission through consumption of raw / undercooked meat, contaminated eggs and milk.
  • Secondary spread can be human - human.
  • Important species:
    • S. typhi
    • S. paratyphi
    • S. enteritidis
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19
Q

Describe the pathogenesis of Salmonella infection.

A
  • Ingestion of large numbers of bacteria.
  • Absorption to epithelial cells in terminal section of the small intestine.
  • Penetration of cells and migration to lamina propria.
  • Multiplication in lymphoid follicles.
  • Inflammatory response mediates release of prostaglandins.
  • Stimulation of cyclic AMP.
  • Release of fluid and electrolytes causing diarrhoa.
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20
Q

Describe the consequences of S. typi and S. paratyphi infections.

A
  • Cause enteric fevers: typhoid and paratyphoid.
  • Systemic infections initiated in gastrointestinal tract.
  • Species restricted to humans.
  • Multiply within, and are transported around the body in, macrophages.
  • Patients can excrete S. typhi in faeces for several weeks after recovery.
  • 1-3% become chronic carriers, most common in women and the elderly.
  • Public health concern: it is a notifiable disease.
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21
Q

What are the available vaccines for typhoid?

A
  • Oral; live attenuated
    • Booster after 5 years
  • Parenteral; capsular polysaccharide
    • Booster after 2 years
  • 50-80% effective.
  • Recommended for travellers to endemic areas.
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22
Q

Describe the characteristics of shigella spp. and name the 4 species.

A
  • Bacillus.
  • Causes shigellosis (bacillary dysentery).
  • Human-only pathogen.
  • 4 species:
    • S. dysenteriae: most serious
    • S. flexneri: severe disease
    • S. boydii: severe disease
    • S. sonnei: mild infections
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23
Q

Describe the pathogenesis of shigella infection.

A
  • Attaches to mucosal epithelium of distal ileum and colon.
  • Causes inflammation and ulceration.
  • Rarely invasive.
  • Produces Shiga toxin (STx).
  • Diarrhoea watery initially, later can contain blood and mucous.
  • Disease is usually self-limiting.
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24
Q

Describe the characteristics of listeria monocytogenes.

A
  • Coccobaccillus.
  • Causes listeriosis.
  • Food-borne pathogen associated with paté, soft cheese, unpasturised milk, hummus.
  • <1000 organisms may cause disease.
  • Population at risk:
    • Pregnant women (with possibility of infection of the baby in utero or at birth).
    • Immunosuppressed individuals (e.g. those with AIDS or on cancer / immunosuppressive drugs).
    • The elderly.
  • Usually presents as meningitis.
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25
Q

Describe the characteristics of antibiotic-associated diarrhoea.

A
  • Does NOT involve ingestion of pathogen or toxin.
  • Can arise from disruption of gut microbiota following antibiotic therapy.
  • Tetracycline - allows colonisation by Staphyloccocus aureus & Candida sp.
  • Clindamycin suppresses gut microbiota and allows Clostridium difficile to multiply - overgrowth.
  • C. difficile infection is now associated with resistance to vancomycin.
26
Q

Describe C. difficile infections.

A
  • Produces spores for survival.
  • Produces an enterotoxin and a cytotoxin.
  • Nosocomial infections largely responsible for increase in cases.
27
Q

Describe Clostridium perfringens infection.

A
  • Usually caused by type A strains from animal guts and soil.
  • Contamination of raw meat products.
  • Spores survive cooking and germination takes place.
  • Multiplication in large intestine, production of spores and enterotoxin.
  • Damage to intestinal epithelium.
  • Diarrhoea.
28
Q

Describe Rotavirus.

A
  • ‘Rota’ = wheel.
  • 11 separate segments of double-stranded RNA.
  • Infects many mammals.
  • Infection commonest in children <2 years old.
  • As few as 10 ingested particles can cause disease.
  • Seasonal ocurrence (commonest in cooler months).
  • Transmission is faeco-oral, but may also be faeco-respiratory.
29
Q

Describe the pathogenesis of rotovirus infection.

A
  • Incubation period of 1-2 days.
  • Replication of virus in small intestinal epithelial cells at tips of villi.
  • Results in villous atrophy.
  • Damage caused to infected cells leaving immature cells with reduced absorptive capacity for sugar, water and electrolytes.
  • Onset of vomiting, diarrhoea lasting 4-7 days.
  • Up to 1010 - 1011 virus particles / gram faeces released.
30
Q

What are the available vaccines for rotavirus?

A
  • RotaRix; RotaTeq
    • Oral administration (2-3 doses)
    • First dose at 6-10 weeks of age
    • Live, attenuated virus
  • Introduced in UK from 2013.
31
Q

Describe norovirus.

A
  • Winter vomiting disease.
  • Accounts for most non-bacterial outbreaks worlwide.
  • Past infection in 60% of adults.
  • Human-only pathogen.
  • Transmission is faeco-oral, contaminated water / shellfish, fomites.
  • <100 virions can establish infection.
32
Q

What vaccines are available for norovirus?

A
  • NONE YET
  • Still ~4-5 years away.
  • Good hand washing instead goes a long way.
33
Q

Describe enteric adenovirus.

A
  • Accounts for 10% of community-acquired diarrhoea in young children.
  • No seasonal incidence.
  • Asymptomatic infections common.
  • Mild, but prolonged diarrhoea.
34
Q

Describe the transmission of intestinal protozoa and helminths?

A
  • Complex life-cycle stages.
  • New infections depend on contact with faecal-derived material.
  • Infection levels reflect hygiene / sanitation standards.
  • Usually acquired through ingestion of contaminated food or water.
  • Symptoms usually present as acute to chronic diarrhoea and inflammation.
  • Occasionally, spread of parasites into other organs may occur.
35
Q

Describe Giardia lamblia.

A
  • Giardiasis is a frequent cause of travellers’ diarrhoea globally.
  • Detected in both drinking and recreational water.
  • Can be passed from person to person.
  • Infective dose is small: 10-25 cysts.
  • Diagnosis by microscopy of stool samples.
36
Q

Describe the life cycle of G. lamblia.

A

​​2 stages:

  • Trophozoite
    • Flagellated and bi-nucleated.
    • Lives in upper part of the small intestine.
    • Adheres to the brush border of epithelial cells.
  • Cyst
    • ​Formed when trophozoite forms a resistant wall.
    • Passes out in stools.
    • Can survive for several weeks.
37
Q

Describe the pathogenesis of G. lamblia.

A
  • Present in the duodenum, jejunum and upper ileum.
  • Attaches to the mucosa via ventral sucker.
  • Does not penetrate the surface.
  • Causes damage to the mucosa and villous atrophy.
  • Leads to malabsorption of food, especially fats and fat-soluble vitamins.
  • May swim up the bile duct to the gall bladder.
38
Q

What are the clinical manifestations of G. lamblia?

A
  • Mild infections are asymptomatic.
  • Diarrhoea is usually self-limiting (7-10 days).
  • Chronic diarrhoea presents in immunocompromised patients.
  • Stools are characteristically loose, foul-smelling and fatty.
39
Q

Describe cryptosporidium parvum.

A
  • Significance grew during the early years of AIDS epidemic (opportunistic infection).
  • Transmission through faecally-contaminated drinking water.
  • Animal reservoir (usually cattle).
  • Infective dose: as few as 10 oocysts.
40
Q

Describe the life-cycle of C. parvum.

A
  • Asexual and sexual development within the host.
  • Ingestion of resistant oocysts.
  • Release of infective sporozoites in the small intestine.
  • Invasion of microvillus border of intestinal epithelium.
  • Division to form merozoites which re-infect cells.
  • Aftersexual phase, oocytes are released.
41
Q

Describe the clinical manifestations of C. parvum.

A
  • Moderate to severe profuse diarrhoea.
  • Up to 25L of watery faeces / day.
  • Usually self-limiting disease.
  • In HIV positive individuals with CD4+ T-cell counts of <100/mm3, diarrhoea is prolonged and may become irreversible and life-threatening.
42
Q

Describe Entamoeba histolytica.

A
  • Common in tropical and sub-tropical countries: prevalent in >50% of population.
  • Transmission via ingestion of contaminated food or water.
  • Transmission also occurs through anal sexual activity.
  • Cysts pass through stomach and excyst in the small intestine giving rise to progeny.
  • These adhere to epithelial cells and cause damage mainly through cytolysis.
  • After mucosal invasion, cysts invade RBCs giving rise to amoebic colitis.
  • Trophozoite stages live in large intestine and pass out as resistant, infective cysts.
43
Q

Describe the pathogenesis of E. histolytica.

A
  • Adheres to epithelium and acute inflammatory cells.
  • Resists host humoral and cell-mediated immune defence mechanisms.
  • Produces hydrolytic enzymes, proteinases, collagenase and elastase.
  • Produces protein that lyses neutrophils, the contents of which are toxic to the host.
44
Q

What are the clinical manifestations of E. histolytica?

A
  • Small localised superficial ulcers leading to mild diarrhoea.
  • Entire colonic mucosa may become deeply ulcerated leading to severe amoebic dysentery.
  • Complications include intestinal perforatin.
  • Trophozoites may spread to the liver, and other organs.
  • Rarely, abscesses spread to overlying skin.
45
Q

What are the protozoal infections of the GI tract?

A
  • G. lamblia
  • C. parvum
  • E. histolytica
46
Q

What are the treatments for C. parvum?

A
  • Nitazoxanide
  • Spiramycin
47
Q

What are the treatments for G. lamblia?

A
  • Mepacrine hydrochloride
  • Metronidazole
  • Tinidazole
48
Q

What are the treatments for E. histolytica?

A
  • Metronidazole
49
Q

What are the ways of preventing protozoal infections of the GI tract?

A
  • Improved hygiene and water supplies.
  • Eating only freshly prepared food served hot.
  • Avoiding salads and fuit which cannot be peeled.
  • Avoiding tap water and ice cubes.
50
Q

Describe nematode intestinal infections.

A
  • Nematodes are the most clinically important intestinal worms.
  • Often soil-transmitted.
  • Infections occur by either:
    • Swallowing infective eggs (Ascaris lumbricoides, Trichuris trichiura).
    • Active skin penetration by larvae and systemic migration through lung to intestine (Strongyloides stercoralis).
  • Diagnosis by stool microscopy.
51
Q

Describe Strongyloides stercoralis.

A
  • Pinworm
  • Disruption of small intestinal mucosa
  • Villous atrophy
  • Marked loss of elasticity of intestinal wall
52
Q

What are the clinical manifestations of S. stercoralis?

A
  • Dysentery (persistent in immunocompromised hosts).
  • Dehydration
  • Malabsorption syndrome
  • Analpruritis
  • Association with appendicitis
53
Q

Describe Trichuris trichirua.

A
  • Whipworm
  • Can live for 3 years in the gut
  • Acquired through ingesting eggs on vegetables
  • 10,000 eggs produced daily
  • 800 million cases worldwide
54
Q

Describe Ascaris lumbricoides.

A
  • Giant roundworm
  • Large thick white worm 20-30cm
  • Females produce approximately 20,000 eggs/day from 65 days after infection.
  • Adults live in the gut for 2 years.
  • Causes 1 million cases per year, with 20,000 deaths.
55
Q

What are the clinical manifestations of A. lumbricoides?

A
  • Allergic reaction in sensitised people.
  • Digestive upsets.
  • Protein / energy malnutrition.
  • Intestinal blockages.
  • Worm may invade mouth, nose etc.
56
Q

Describe Enterobius vermicularis.

A
  • Threadworm.
  • Small cylindrical nematodes <1cm.
  • Female migrates to anus at night to lay approximately 10,000 eggs, which may develop to infective stage within hours.
  • Intense itching, secondary bacterial infection - mild catarrhal inflammation and diarrhoea, slight eosinophilia.
57
Q

Describe Ancyclostoma duodenale.

A
  • Hookworm.
  • Often picked up walking barefoot in infected areas.
  • Attaches to small intestine, suck blood and protein, often present in huge numbers.
  • Cause hypochromic anaemia.
  • Blood loss 0.03ml/day/worm (often 500-1000 worms).
58
Q

Describe Taenia solium (tapeworm).

A
  • Acquired from ingesting worms or eggs in undercooked pork.
  • Reside in large intestine.
  • Can grow up to 7m long.
  • Scolex - for attachment.
59
Q

Describe the treatment and prevention of intestinal helminth infections.

A
  • Improved hygiene and sanitation are important in prevention of infection.
  • Specific drugs:
    • Mebendazole
    • Praziquantel
    • Ivermectin
    • Piperazine
60
Q

There are antiprotozoal and antihelminthic agents. What are the particular problems posed when treating with these?

A
  • Pose particular problems because of:
    • Large variety of species
    • Complexities of their life cycles
    • Differences in their metabolic pathways
    • Drugs active against protozoa are inactive against helminths
61
Q

Describe the use of oral rehydration therapy (ORT) in treatment of intestinal infections.

A
  • Involves the replacement of fluids and electrolytes lost during diarrheal illness.
  • 90-95% of cases of acute, watery diarrhoea can be successfully treated with an oral rehydration solution (ORS).
  • ORS increases the resorption of fluids and salts into the intestinal wall.

Gastrointestinal (10 decks)

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