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Med Micro 2 > Week 2-3: GIT Infections > Flashcards

Week 2-3: GIT Infections Flashcards

1
Q

Dysentery

A

Inflammatory disorder of GIT, usually resulting from disease of the large intestine. Often associated with blood and pus in the faeces. Accompanied by symptoms of pain, fever, abdominal cramps.

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2
Q

Diarrhoea

A

Abnormal faecal discharge characterised by frequent fluid stool, usually resulting from disease of the small intestine and involving increased fluid and electrolyte.

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3
Q

Define: enterocolitis

A

Inflammation involving mucosa of both small and large intestine

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4
Q

Organisms that cause inflammatory diarrhoea, incl. dysentery

A

Bacteria: Shigella spp., Enteroinvasive E. coli, EHEC E. coli, Salmonella enterica, C. jejuni, V. parahaemolyticus, C. difficile.
Viruses: none
Parasites: E. hystolytica

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5
Q

Organisms that cause non-inflammatory diarrhoea

A

Bacteria: ETEC E. coli, enteroaggregative E. coli, V. cholerae.
Viruses: norovirus, rotavirus, enteric adenovirus, astrovirus
Parasites: Giardia, Cryptosporidium spp., microsporidia (fungi)

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6
Q

Inflammatory diarrhoea involves small or large intestine?

A

Large (Colon)

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7
Q

Non-inflammatory diarrhoea involves small or large intestine?

A

Proximal small intestine/bowel

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8
Q

True or false:

In inflammatory diarrhoea, leukocytes are often found in the blood.

A

True

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9
Q

True or false:

In non-inflammatory diarrhoea, leukocytes are often found in the blood.

A

False.

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10
Q

Organisms associated with diarrhoea with systemic disease

A

Bacteria: Salmonella enterica serotype Typhi, Y. enterocolitica, Campylobacter spp.
Viruses: none
Parasites: none

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11
Q

Is diarrhoea with systemic disease associated with small or large intestine?

A

Involves distal small intestine

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12
Q

Leukocytes in the stool:

Inflammatory diarrhoea, incl. dysentery vs. non-inflammatory diarrhoea vs. diarrhoea w/ systemic disease

A

Inflammatory diarrhoea (incl. dysentery): leukocytes often found in blood
Non-inflammatory diarrhoea (usually no leukocytes found in the blood)
Diarrhoea w/ systemic disease: leukocytes may be present in stool

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13
Q

Defence mechanisms in the GIT

A
  1. Mechanical: movements of villi, peristalsis, mucous. Inner layer of mucous is resistant to bacterial penetration, providing protection to epithelial surface.
  2. Chemical: pH of stomach
  3. Immunological: produced by B cells, IgA is trancytosed across epithelium and binds toxins and bacteria in the lumen of the stomach, preventing adhesion to epithelium.
  4. Normal flora restricts pathogens from attaching, obtaining nutrients and oxygen
    3.
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14
Q

Mucous is secreted by a) _____ cells in b) _____.

A

a) goblet b) crypts

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15
Q

Mucous covers the a) _____ cell layer. Secreted mucous forms two layers. It consists of a b) _____ layer on top of an c) _____ layer. Mucous is thick in the d) _____ and e) _____ and thinner in the f) _____. The g) MUC2 mucin molecule is concentrated in h) _____ and i) _____, whereas the MUC5AC mucin is concentrated in the j) _____.

A

a) epithelial
b) outer, non-attached mucus
c) stratified, inner, firmly attached mucus
d) stomach
e) colon
f) duodenum
g) MUC2
h) small intestine
i) colon
j) stomach

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16
Q

Vibrio cholerae virulence mechanisms

A

V. cholerae attach to intestinal epithelium through type IV pili. V. cholerae produce cholera cytotonic enterotoxin, composed of A and B subunits. B subunit binds to the GM1 ganglioside, facilitating uptake of the toxin. A subunit causes an increase in cAMP, which affects the flow of Na2+ and Cl- ions across the epithelium cells, leading to an excess of water excreted into the gastrointestinal lumen, causing diarrhoea.

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17
Q

Six mechanisms of disruption of epithelial barrier leading to diarrhoea

A
  1. Increase Cl- secretion through CFTR (as by cholera toxin)
  2. Decrease Na+ absorption owing to inhibition of Na+/H+ exchanger 3 (as by cholera toxin, heat labile toxin of E. coli)
  3. Downregulation of Na+/glucose co-transporter (as by EPEC.
  4. Direct inhibition of aquaporins (e.g. EPEC)
  5. Disruption of epithelial barrier function by opening of the tight junctions (triggered by inflammatory signalling in epithelial cells (as by EPEC, Yersinia spp., H. pylori)
  6. Destruction of epithelium by invasive pathogen (e.g. Campylobacter)
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18
Q

Six pathotypes of diarrhoeagenic E. coli and symptoms they cause

A
  1. Enterotoxigenic E. coli (ETEC) - watery diarrhoea
  2. Enteropathogenic E. coli (EPEC) - non-specific gastro
  3. Enterohaemorrhagic E. coli (EHEC) - bloody diarrhoea
  4. Enteroinvasive E. coli (EIEC) - dysentery
  5. Enteroaggregative E. coli (EAEC) - watery diarrhoea
  6. Diffusely adherent E. coli (DAEC)
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19
Q

Reasons to request stool cultures

A
  1. Patient is immunocompromised
  2. Patient has recently travelled to a resource poor country
  3. Presence of blood in stool
  4. Diarrhoea present for more than 3 days
  5. Diarrhoea has required intravenous rehydration
  6. Fever is present (indicates invasive pathogen)
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20
Q

What does stool with blood or mucous suggest?

A

Bacterial cause (leukocytes on microscopy)

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21
Q

What does frequent watery stool suggest?

A

Viral gastro

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22
Q

What does a long duration of gastrointestinal illness suggest?

A

Parasitic or other cause

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23
Q

What does a long duration of gastrointestinal illness suggest?

A

Parasitic or other cause

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24
Q

What does decreased urination frequency suggest?

A

Dehydration

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25
Q

Recent antibiotic use in a gastrointestinal infection is indicative of which pathogen?

A

C. difficile

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26
Q

Which pathogens should be considered if there is history of travel to endemic areas in a GIT infection?

A

Cholera or parasitic infections

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27
Q

General workflow of diagnosing GIT infection

A
  1. Rule out bacterial cause (bacterial enteritis usually more severe.
  2. History of travel/untreated water source - examine stool for parasites, and/or if history of travel to endemic areas TCBS (cholera)
  3. Generally assume that lactose fermenters e.g. E. coli are not pathogenic
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28
Q

GIT disease due to preformed toxins is usually caused by which organisms?

A

Staphylococcus aureus
Bacillus cereus
Clostridium botulinum
Clostridium perfringens

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29
Q

Staphylococcus aureus characteristics

A 
– Gram-positive cocci
– Facultative anaerobe
– Nonsporeforming
– Often β-haemolysis on blood agar plates
– Natural habitat - humans (found in anterior nares of about 20% of population persistently, about 60%
intermittently)
– Non-motile
– Catalase positive
– Oxidase negative
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30
Q

Which organism is usually the cause of food poisoning in salty/fatty food such as milk and cheese?

A

S. aureus

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31
Q

Symptoms and characteristics of S. aureus food poisoning

A

– Symptoms: vomiting, fever
– Relatively quick incubation (1-4 hours) due to preformed toxin
– Recovery in 12 hours
– Usually mild and self-limiting

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32
Q

Sources of S. aureus infection

A

– Food handler: Staphylococcus lesion, colonised skin (e.g. eczema), nasal carriage (poor personal hygiene)
– Food: grows in a wide assortment of food; usually appears normal, growth favoured by high lipid content, withstands high salt levels that do not support the growth of most other bacteria

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33
Q

Characteristics, pathogenesis and detection of Staphylococcal enterotoxins

A

– Pyrogenic (fever-causing): due to superantigen activity; crosslink MHC class II and TCR causes non-specific activation of T cells leading to cytokine release and fever
– Emetic (vomit-inducing): stimulates vagus nerve, transmitted to CNS, induces vomiting
– Resistant to heat (can outlast the bacteria that produced them)
– Resistant to proteolytic enzymes in the gut
– Pathogenesis: toxins released into the gut, cross the epithelial barrier and bind cells such as MHC class II expressed by fibroblasts underneath epithelium. This triggers a strong production of cytokines which activates T cells, leading to increased chemotaxis of immune cells into the area which causes further inflammation leading to pain and increased motility. Effects of this include diarrhoea and vomiting.
– Detection: using enzyme immunoassays (EIA), latex assay not as sensitive, molecular typing (subtype of S. aureus strain) for outbreaks

34
Q

Source of Bacillus cereus

A

Grains (e.g. rice)

35
Q

Characteristics, incubation period and diagnostic attributes of Bacillus cereus

A

– Gram positive rods in chains
– Facultative anaerobe
– Produces heat-resistant spores
– Produces emetic toxin (ETE): small peptide, heat-resistant, stable to pepsin and trypsin causing nausea, vomiting with short incubation (1-6 hours) and heat-labile enterotoxin (Nhe) causing diarrhoea with long incubation (8-16 hours)
– Diagnostic characteristics: motile; catalase positive; indole negative

36
Q

Characteristics of Clostridium botulinum

A

– Gram-positive anaerobic bacillus
– Spore bearer; subterminal oval endospores survive heat treatment (survive canning, processing, cooking).
– Grows best in non-acid foods (pH>4.5)
– Produces highly potent A/B exotoxin (destroyed by boiling).
– Diagnostic characteristics: Motile; EYA Lecithinase + or -ve; lipase positive

37
Q

Infant botulism: cause, pathogenesis, characteristics, symptoms

A

– Cause: Clostridium botulinum, and affects infants 5-20 weeks of age that have been exposed to solid foods.
– Characterised by constipation, weak sucking ability and generalised weakness
– C. botulinum can establish itself in the bowel of infants at a critical age before the establishment of competing intestinal bacteria

38
Q

Foodborne botulism: cause, pathogenesis, characteristics

A

– Cause: Clostridium botulinum
– Characteristics: Symmetrical descending paralysis (cranial nerves, then muscles in lower parts of body)
– Severity depends on amount of toxin ingested
– Frequently fatal, especially if diagnosis is delayed (first cases in an outbreak)
– Symptoms: double/blurred vision, droopy eyelids, slurred speech, difficulty swallowing, dry mouth, muscle weakness

39
Q

Mechanisms of Botulinum toxin

A
  1. Highly potent A/B exotoxin is absorbed from stomach and enters the blood stream
  2. Toxin targets peripheral nerve endings and blocks release of acetylcholine from vesicles
  3. Results in flaccid paralysis and can cause irreversible damage to nerves
40
Q

Management of patients with botulism

A

– Polyvalent antiserum - Ab that will interfere with the binding of the toxin. Occasional adverse (e.g. anaphylactic) reactions to antiserum are possible
– BabyBIG (botulism immune globulin)

41
Q

Characteristics, pathogenesis and incubation period of Clostridium perfringens

A

– Gram positive rods
– Anaerobic endospore bearer; spores survive cooking and germinate in food
– Natural habitat: soil, water
– Mesophile, optimal 37C
– Several types exist, based on range of toxins. Type A is most common. Enterotoxin produced when bacterium sporulates. Induced by low pH in the stomach, causes diarrhoea and abdominal pain.
– Recovery: 1-2 days
– Incubation period: 10 hours - not preformed toxin, needs time to sporulate
– Diagnostic characteristics: usually motile; catalase negative; oxidase negative

42
Q

Source of C. perfringens

A

Soil, faeces, often found in improperly cooked or stored meat

43
Q

C. perfringens epsilon toxin mechanism

A

Acts in the small bowel and alters electrolyte transport systems through formation of large complexes in the membrane of intestinal epithelial cells. This leads to damage of cell walls, unbalanced potassium efflux and diarrhoea. No mucosal damage occurs.

44
Q

Shigella are closely rated to which organism?

A

E. coli

45
Q

Epidemiology of Shigella infections

A

– Human only disease
– High infectivity: 1-2 organisms can establish infection
– No carrier state, nonsporeforming, poor survival in environment (direct contact with faeces needed for infection)

46
Q

Transmission of Shigella

A

Person to person, occasionally food (not common), low infective dose determines mode of transmission.

47
Q

Clinical presentation of Shigella

A

– Incubation period 36-72 hours
– Range of severity. Complications only with S. dysenteriae, causing CNS disturbances and haemolytic uremic syndrome characterised by blood in stools due to large bowel damage, and renal failure
– Symptoms: watery diarrhoea followed by dysentery (stool containing mucous and blood), fever, abdominal cramps
– Recovery in 2-7 days

48
Q

Pathogenesis and pathology mechanisms of Shigella

A

Pathology mechanisms:

  1. Shigella cannot enter epithelial cells from gut lumen. Shigella are able to pass epithelial cell layer by transcytosis through M cells (no receptors required), avoid degradation by macrophages by inducing apoptosis-like death accompanied by proinflammatory signalling.
  2. After release from macrophage, Shigella are exposed to the basolateral membrane of epithelial cell and use type III secretion system to inject virulence proteins, causing rearrangement of actin, allowing Shigella to enter the cell.
  3. Inside the epithelial cell, protein IpaB lyses the phagosome membrane and Shigella is able to escape into cytoplasm where it multiplies.
  4. IcsA, a surface-exposed outer membrane protein located at one end of the bacterium, causes rapid polymerisation and de-polymerisation of host cell actin, propelling bacteria through cell cytoplasm to cell junction.
  5. Shigella interacts with host cell molecules to form protrusions in host cell membranes. IcsB on the bacterial surface lyses protrusions formed by bacterium and the bacterium is able to pass through into the next cell.

Pathogenesis:
– Low infective dose; resistant to stomach acid
– Major mechanism of Shigella infections is ability to invade and grow in colonic epithelial cells, eventually leading to epithelial cell death.
– Infected epithelial cells die
– Strong inflammatory response
– Ulcers of colon
– Intracellular location protects bacteria from host humoral and cell-mediated immunity
– Watery diarrhoea could be enterotoxin-mediated as well as due to epithelium damage
– Dysentery due to invasion and death of enterocytes, causing shallow ulcers that bleed

49
Q

Leading causes of diarrhoeal death

A
  1. Rotavirus 2. Shigella
50
Q

Shiga toxin characteristics and pathogenesis

A

Characteristics:
– Produced by Shigella dysenteriae and EHEC only
– Protein exotoxin (liberated by multiplying bacterium), extremely potent, heat labile
– A-B structure (B - binding, A - inhibition of protein synthesis)
– Haemolytic uraemic syndrome (HUS)
Pathogenesis:
– Damage to endothelium of blood vessels, causing damage following bloodstream spread to kidney (renal failure), brain (neurological implications), gut capillaries, pancreas etc.

51
Q

Treatment for Shigella

A

– Mild cases: oral fluids and electrolytes
– Severe cases: Intravenous fluids and electrolytes
– Antibiotics controversial (not always effective; local resistance develops quickly), need to know resistance profile

52
Q

Pathogenesis of Salmonella

A

Pathogenesis
– High infectious dose required to cause illness
– Some bacteria killed by stomach acid
– Passes through stomach
– Attaches to and enters cells of small intestine and colon
– Multiplies in submucosal area in the lymphoid follicles
– Causes acute inflammation: influx of neutrophils, +++ neutrophils in stools (due to innate immune recognition, similar for all inflammatory type diarrhoeas). This host response usually stops further spread; no further than mesenteric lymph nodes i.e. usually no bloodstream invasion (unless immuocompromised pa9ent)

53
Q

Which Salmonella serovars cause gastroenteritis?

A

S. enterica serovar Typhimurium

S. enteriditis

54
Q

Epidemiology of Salmonella gastroenteritis

A

– Source: usually animal, can be found in dairy
– Vehicle usually food
– Humans excrete for 1-2 weeks after infection
– No long-term carrier state
– Occasional transmission from person-person via faecal-oral route

55
Q

Pathogenesis of Salmonella

A

– High infectious dose required to cause illness
– Some bacteria killed by stomach acid
– Food mass protects Salmonella allowing passage into the small intestine
1. Salmonella can directly enter intestinal epithelial cells by the apical pole of the cell or through luminal capture by dendritic cells that emit pseudopods between epithelial cells, allowing systemic dissemination. More frequently, Salmonella enter the subepithelial space through transcytosis by M cells of the follicle-associated epithelium (mainly in Peyer’s patches of the ileal portion of the small intestine but also in the colon), entering the subepithelial space after phagocytosis by macrophages.
2. Through SP1I1 type III secretory system, Salmonella inject effector proteins into the cytoplasm of the epithelial cell; SopE/SopE2, SigD, sptP promote actin rearrangement, and uptake of salmonellae into the cell, and SseJ, SptP and SipC interact with microtubules and intermediate filaments to maintain structure of Salmonella-containing vacuole.
3. From the endocytic vacuole, Salmonella inject SPI2 effector proteins using T3SS2, allowing intracellular survival within phagocytes and is important for systemic spread and the colonisation of host organs. This prevents phagolysosomal fusion, allowing growth and survival as well as inducing macrophage apoptosis, triggering IL-1β production and subsequent inflammatory response. Released Salmonellae can now either enter epithelial cells through the basolateral side of the epithelial cells or disseminate systemically. Damage to the epithelial cells leads to a leaky barrier, causing diarrhoea with high neutrophils count.

56
Q

Symptoms of Salmonella gastroenteritis

A

– Clinical symptoms exhibit an incubation period of 1-2 days
– Symptoms include nausea and vomiting followed by diarrhoea and fever.
– Duration of 3-5 days until complete recovery

57
Q

Treatment for Salmonella gastroenteritis

A

Fluid and electrolytes

Antibiotics if septicaemia is present

58
Q

Strategy for isolation of enteric pathogens from faeces

A
  1. Faecal samples directly plated onto MAC/HBA split to distinguish lactose fermenters. Faecal samples are also inoculated in an enrichment broth that promote the growth of Salmonella/Shigella and inhibit growth of intestinal flora (e.g. Selenite F) for 8-12 hours and subcultured onto differential/selective (e.g. XLD, DCA, HEK). Lactose fermenters are discarded.
59
Q

Characteristics of Campylobacter

A

– Gram negative curved rods
– Nonsporeforming
– Microaerophillic (5% O2)
– Most pathogenic species are thermophillic
– Exhibit darting motility - move in corkscrew fashion
– Coccoid forms develop in older cultures - viable but non-culturable form

60
Q

Transmission of Campylobacter

A

Transmission to humans occurs by:
– Ingestion of contaminated food or water, including
unpasteurized milk and undercooked poultry.
– Direct contact with faecal material from infected animals or persons

61
Q

Symptoms of Campylobacter infection

A

– Campylobacter infection may be subclinical or cause disease of variable severity
– C. jejuni infection typically results in abdominal pain, fever and diarrhoea which may be mucopurulent or bloody.
– Symptoms usually last 2-5 days
– An unusual manifestation of Campylobacter infection is Guillain-Barre syndrome; during infection antibodies against neuronal surface-gangliosides are produced due to antigenic mimicry between LPS and and GM1 human gangliosides, leading to polyneuritis.

62
Q

Pathogenesis of Campylobacter infection

A

– Low infectious dose required to cause illness: 100 bacteria
– C. jejuni killed by stomach acid
– Food mass protects Campylobacter, allowing passage through stomach
– Main site of colonisation: jejunum, colon may also be involved.
– Penetrates mucosa and invades lamina propria
– Virulence factors: LPS (triggers inflammation), flagella, cytotoxins, haemolysins, secreted protease HtrA, phospholipase A
Molecular mechanisms:
1. Campylobacter are repelled by bile and undergo chemotaxis towards muffins, glycoproteins and acids, attach to epithelial cells via the flagella to an unknown receptor.
2. Campylobacter outermsmbrane protein CadF binds to epithelial extracellular matrix protein fibronectin, leading to adherence to the epithelial cell.
3. Concurrently, Campylobacter secrete HtrA which breaks down tight junctions, allowing paracellular migration and parabasal infection.
4. CadF-fibronectin binding causes a cascade which leads to actin remodelling and vacuole-internalisation of Campylobacter.
5. Campylobacter produce cytolethaldistending toxin (CDT) which blocks transition to G2 phase, causing cell death.
6. Epithelial cell death exposes the submucosal layer, leading to blood in the stool.

63
Q

Treatment for management of patients with Campylobacter infection

A

– Mild cases: fluid replacement only

– Severe cases: erythromycin or clarithromycin

64
Q

Diagnosis of Campylobacter infection

A

– Selective media (e.g. Skirrows supplement)
– Catalase positive
– Hippurate hydrolysis

65
Q

Viral gastroenteritis clinical signs and symptoms

A

Children:
– Incubation: 24-48 hours
– Diarrhoea, vomiting, +/- fever
– Dehydration a concern in young children
– Lasts for up to 1 week, resolves completely
Adults:
– Incubation period: 24-48 hours
– Diarrhoea, nausea, vomiting, +/- fever
– Complete resolution: 12-60 hours
Viral gastroenteritis cannot be distinguished from bacterial diarrhoea

66
Q

Most common causes of gastroenteritis in children under 5

A

Most common: rotaviruses. Followed by Adenovirus types 40,41

67
Q

Most common causes of viral gastroenteritis in adults

A

Noroviruses

68
Q

Most common cause of gastroenteritis in babies and young children

A

Astroviruses

69
Q

Treatment for viral gastroenteritis

A

No antiviral drugs available. Treatment includes fluids (intravenous if necessary). Dehydration is a particular concern in infants.

70
Q

Rotavirus characteristics

A

– Icosahedral symmetry
– dsRNA
– Double layered capsid
– Segmented genome; re-assortment can occur, leading to creation of new viruses
– Two serotypes affect humans
– Other serotypes affect different animal species and can occasionally affect humans

71
Q

Rotavirus gastroenteritis - epidemiology and clinical presentation

A

– Most common cause of gastroenteritis for children under 5 years
– Adults occasionally (IgA immunity)
– Virus shedding 2-5 days after onset
– Infective dose: 10 virions
– Stable in environment, resists drying
– Incubation 1-2 days
– Acute onset
– Symptoms include: vomiting (projectile), diarrhoea, fever. Often respiratory symptoms as well
– Dehydration is of concern particularly in young children
– Can be fatal if fluid replacement is not available
– Duration up to one week until complete recovery

72
Q

Rotavirus - pathogenesis

A
  1. Ingested virus survives stomach acid
  2. Rotavirus adheres to columnar epithelial cells at tips of villi in small intestine through spike protein VP4, promoting uptake of virus into the cell.
  3. Virus replicates inside epithelial cell, exiting via trancytosis and infecting neighbouring cells.
  4. Infected cells are damaged and lost, leaving immature cells with reduced absorptive capacity leading to fluid accumulation and increased osmotic pressure in lumen causing diarrhoea and dehydration. NPS4 toxin also induces secretory diarrhoea through Ca2+-dependent secretion by intestinal cells or through Cl- secretion.
  5. Pathogenesis is abated due to antibody production against surface Ag on virus and toxin and infection resolves.
    – Virulence factors include VP4 spike protein (adhesin) and NSP4 toxin.
73
Q

Host defence against rotavirus

A

IgA the most important defense
– IgA in colostrum, mother’s milk reduces severity
– After ~ 1 week, IgA produced in response to infection
– Symptoms relieved
– Villi regenerate
– Complete recovery

74
Q

Rotavirus diagnosis

A

– Very large numbers of rotavirus in stools.
– Latex agglutination or ELISA is used for antigen in stools; rapid and inexpensive. If positive, no need for bacteriological investigation.
– Cell cultures are difficult, not used diagnostically

75
Q

Rotavirus vaccine

A

– Live attenuated oral vaccine, given in several doses at 2, 4, and 6 months
– Some babies shed virus for 1 week after 1st dose, risk to immunocompromised individuals
– Side effects are rare but include intussusception and anaphylaxis

76
Q

Characteristics of Norovirus

A

– ssRNA virus
– Capsid
– No envelope
– Cannot be grown in culture using standard methods

77
Q

Epidemiology and Clinical presentations of norovirus

A

– Common source - shellfish, water
– Highly infectious, person-person spread after first cases identified
– Incubation 1-2 days
– Acute onset
– Nausea, vomiting, diarrhoea, abdominal pain, +/- fever, chills, pains, headache
– Complete recovery in 24-48 hours

78
Q

Pathogenesis of norovirus

A

– Causes blunting of villi, similar to rotavirus
– Damage to intestinal wall causes inflammation and diarrhoea
– Shedding for ~2 weeks

79
Q

Diagnosis of norovirus

A

– Reverse transcriptase PCR of stool or vomitus mainstay of diagnostic tools
– ELISA-based kits are available to detect viral particles in stool
– Has not been grown in cell culture

80
Q

Adenovirus characteristics

A

– Large dsDNA virus
– Icosahedral
– Non-enveloped
– Resistant to inactivation by disinfectants
– Types 40, 41 cause gastroenteritis in children

81
Q

Epidemiology and clinical presentation of adenovirus infection

A

– Second most common cause of childhood diarrhoea
– Clinical presentation similar to rotavirus but milder
– Tranmission child-child
– Large numbers in stools of infected children

82
Q

Lab diagnosis of adenovirus

A

– Viral DNA detected in stools by PCR

– Rapid ELISA tests detect viral antigen found in stools

Med Micro 2 (8 decks)

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