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Term 3/4 Flash Cards > Micro - GIT > Flashcards

Micro - GIT Flashcards

1
Q

Colonization of GIT from before birth

A
  • Before birth - Gut is sterile
  • Immediately after birth - E. coli & Streptococci appear
  • 4 days after birth - Facultative anaerobes create reducing environment. Bifidobacterium appear, possibly Bacteroides & Clostridium spp.
  • Breast-fed - E. coli, Streptococci, Bacteroides & Clostridium #’s decline. Bifidobacterium #’s remain high
  • Formula-fed - Lactobacilli present
  • Beginning of weaning from breast-fed - E. coli, Streptococci & Clostridium #’s return to high levels Flora now similar to Formula fed infants
  • After weaning (breast and formula) - Bacteroides & anaerobic Gram positive cocci gradually increase in #’s
  • After completion of weaning - conversion to adult flora
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2
Q

Normal flora of mouth

A

– Streptococcus, Neisseria, Actinomyces, Veillonella &
Lactobacillus, some yeasts, transient viruses

– Eruption of 1st teeth: Porphyromonas, Prevotella &
Fusobacterium

– Growth of Teeth: S. sanguis, S. mutans & S. salivarius *Dental plaque

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3
Q

Normal flora of stomach

A

Sterile

OR

10^3 bacteria: Streptococcus, Staphylococcus, Lactobacillus & Peptostreptococcus

N.B. 10^5-10^7 bacteria/ml: abnormality (achlorhydria or malabsorption syndrome)

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4
Q

Duodenum

A

Fluctuating transients: aerobic Streptococci, Staphylococci,
Lactobacilli, yeasts

N.B Complete absence of coliforms & Bacteroides

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5
Q

Jejunum-ileum

A

– High counts Enterobacteriaceae

– Some Streptococcus, Staphylococcus, Lactobacillus, Bacteroides, Bifidobacterium, Clostridium

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6
Q

Large intestine

A

95-99% Anaerobic: Bacteroides, Bifidobacterium, Eubacterium, Peptostreptococcus & Clostridium Plus Enterobacteriacea

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7
Q

Food poisoning: toxemia/non-inflammatory gastroenteritis - consumption of food containing toxins

A

ONLY:

  • C. botulinum, S. aureus, B. cereus (1 form)
  • Fungal - Wild Mushrooms (Amanita, Clitocybe & Psilocybes) Aflatoxin (Aspergillus sp.)
  • Marine toxins - Ciguatera, Scromboid & “Shellfish”

Ingestion of preformed toxins (NOT INFXN). NO microbial growth w/in human GIT
Symptomology: usually rapid (minutes-hours) (C. botulinum: 6hrs-8days) -> exception
Lack of fever; no faecal leukocytes

Toxins Affect:
CNS (C. botulinum)
Both CNS & Intestines (S. aureus & B. cereus)

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8
Q

Staph aureus

A

Aerobic or facultative. Coagulase +ve, Catalase +ve

• Produces 8 Exotoxins (A, B, C1, C2, C3, D, E, H) Water-soluble, low mw proteins, ST (chromosomal)
• Frequently implicated A & D singly or combination
• Neurologic (vomiting) & Enteric (diarrhoea) effect
• Mode of action:UNKNOWN
– act on gut receptors; stimulate vomiting (vagus & sympathetic nerves)
– NO stimulation of adenylate cyclase

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9
Q

Staph aureus clinical

A
  • Self-limiting illness. Some EMESIS w/in 6hr ingestion (mean 4.4hr) (BUT Not all vomit)
  • Recovery 24-48 hours
  • Other Common Sx’s:nausea, abdominal cramps, diarrhoea (watery), HA’s, muscular cramping and/or prostration

• Incriminated Foods: cooked meat (fish, poultry), bakery foods (cream-filled), dairy produce, fruit, vegetables & salads. Poor Handling of Food

• Incidence
Highest: Summer
2nd: November/December: Holiday period

Dx: confirm w/coagulase test

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10
Q

Bacillus cereus

A

Gram +ve rods. Arranged in chains. Aerobic or facultative. Spore former
Emetic toxin & Enterotoxin Habitat: air, soil, water & dust

• Pathogenesis: short incubation. 
ST Neurotoxin (peptide) prodn by cells in food
Incriminated Foods: rice & pulses

• Non-selective medium: Blood agar (sometimes + polymyxin (suppress Gram-ve)

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11
Q

Clostridium botulinum

A

Variable size Gram +ve rods. Anaerobic
Ferment range of CH2O’s. Gas Spore former
Produce exotoxins. Susceptible to PCN
Habitat: soil (fertilized animal excreta), lower GIT humans & animals

• Food poisoning - Originally: contaminated meat (sausage)
Now: Home-canning, vegetables, fish, fruits & condiments
• Infant

PATHOGENESIS: NEUROTOXIN
• 8 types (A, B, C1, C2, D, E, F, G) Proteins. Toxin A (potent) 10-8g KILL HUMAN
• Humans: A, B, E, rarely F (Animals: C & D)
• U.S frequent isolate type A, then B & E
• Europe frequent isolate type B (A rare)

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12
Q

Food poisoning botulinum

A

• Clinical sx’s vary
Incubation time: commonly 18-36hr. Mild illness (disregarded or misdiagnosed). Serious dz (fatal within 24hr)

Includes: nausea, vomiting & abdominal pain Diarrhoea often present: Constipation may occur
• GI disturbances
1/3 patients (toxin A or B) & Almost all toxin E
Toxemia symptoms then apparent
No fever in absence of complicating infections

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13
Q

Botulism dx

A

• Fatal toxemia (rule out botulism)
• REPORTABLE DISEASE
• Presumptive dx:
– Presence of rapidly descending paralysis
– Ingestion of home canned or fermented food?
• Confirmative dx
– Demonstration of botulinum toxin in serum/faeces or incriminating food (mouse toxin-neutralization test)

  • GBS: ascending paralysis. Paresthesias or other sensory abnormalities, elevated CSF protein
  • MG: descending paralysis. Mm fatigability during exercise and positive response to endrophomium
  • Other microbial food poisonings & gastroenteritis – No CN involvement
  • Chemical (& non-microbial) food poisonings – Sx’s occur w/in minutes
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14
Q

Infant botulism

A

(PLEASE NOTE: NOT Food Poisoning)
• Infants (2 wks-6 mos)
• Spore Germination (GI tract) -> Vegetative cells -> REPLICATE & THEN release toxin
• Implicated Types A & B

Sx’s: illness & constipation (overlooked)
• Proceeds: lethargy, sleeps more than normal. Suck & gag reflexes diminish. Dysphagia becomes evident as drooling
• Later: Head control lost. Infant becomes flaccid
• Severely Infected: Respiratory Arrest

Dx: difficult
• Requires: prompt action for survival. Differential Dx: neurological + GI Toxin. Demonstration in faeces
• Txt: Botulism Antitoxin Heptavalent (A, B, C, D, E, F, G)-
(Equine)
Supportive measures: maintain respiration
Baby Botulism Immune Globulin (BIG-IV) for A & B toxins

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15
Q

Mushroom (fungal) toxin

A

• NOT COMMON
• Short-acting: Wild mushrooms
Toxin: Museinol, Muscarine, Psilocybin, Coprius artemetaris, Ibotenic acid
Incubation <2hrs: Vomiting, diarrhoea

• Long-acting: Mushrooms (uncultivated) Toxin: Amantia. Incubation 4-8hrs: Diarrhoea, abdominal cramps. CAN BE FATAL

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16
Q

Mycotoxigenic fungi

A
  • Mycotoxins: 2ndary metabolites. Aspergillus, Fusarium & Penicillium
  • AFLATOXINS: Aspergillus flavus & A. parasiticus. Under favourable conditions (temp & humidity)
  • Contamination of: tree nuts, peanuts, oilseeds (corn & cotton)
  • Responsible for: acute necrosis, cirrhosis & carcinoma (liver)
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17
Q

Ciguatera poisoning

A

Caribbean/Tropical Pacific. Dinoflagellates: Gambierdiscus toxicus: Ciguatoxin

Large predatory reef fish: barracuda, grouper & amberjacks

• Acute GI symptoms: 3-6hrs after ingestion
Watery diarrhoea, nausea, abdominal pain (12 hr)

• Neurologic sx’s: circumoral & extremity paresthesia, severe pruritus, hot/cold temp reversal

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18
Q

Scromboid poisoning

A

Non-allergic histamine, Bacteria: Stenotrophomonas maltophilia, M. morganii
Histadine -> Histamine (Scrombotoxin)

Scrombridae Fish: tuna, mahi-mahi, marlin & bluefin.

  • Burning sensation in mouth, a metallic taste
  • Acute GI sx’s: mins-3hrs after ingestion (<1hr) Watery diarrhoea, nausea, lasting 3-6hrs
  • Other symptoms: dizziness, urticaria (rash), facial flushing, generalised pruritus, paresthesias
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19
Q

Brevetoxins

A

Neurologic shellfish poisoning. Dinoflagellate algae: Karenia brevis

• Incubation: <1-3 hours; Duration: 24-73 hours
• Paresthesia, mouth numbness, tingling sensation of
mouth & extremities, GI upset

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20
Q

Saxitoxins

A

Paralytic shellfish poisoning. Dinoflagellate algae: Alexandrium spp., Gymnodinium catenatum, Pyrodinium bahamense, Gonyaulax spp.

• Incubation: s less common, ataxia (muscular in-coordination). Severe cases: muscular paralysis, respiratory paralysis

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21
Q

Non-inflammatory diarrhea - food associated: foodborne infection

A

Ingestion of organisms present in food
Toxins produced once colonised GI tract (bacteria) (NO bacterial INVASION)

Symptomology: Acute watery diarroea. Longer incubation due to colonization. With/without fever

Toxins Affect: Enterotoxins (bacteria)

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22
Q

Escherichia coli

A
  • Family Enterobacteriacea. MOST COMMON Gram -ve bacilli (Rods) facultative anaerobes!
  • Part of normal commensal intestinal flora. Considered major opportunistic pathogen. Only virulent after bacteriophage
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23
Q

ENTEROTOXIGENIC E. coli (ETEC)

A

Transmission: contaminated food & water. Infective dose: 100 million - 10 billion cells
Primary cause of “Traveller’s Diarrhea”

Pathogenesis: 2 stages

  1. E. coli adheres to brush border of SI using special fimbriae colonization factor Ags (CFAs)
  2. Make one or both of plasmid-encoded ENTEROTOXINS

Enterotoxins: AB toxins.
LT: Similar to Cholera. Binds to GM1 rec -> toxin enter cell -> increase AC -> increase cAMP -> outflux of H2O and electrolytes
ST: guanylate cyclase

Sx’s: nausea, vomiting, malaise. Primary tx is rehydration

24
Q

ENTEROPATHOGENIC E. coli (EPEC)

A

“Infantile Diarrhoea.” Childhood Diarrhoea. Developing countries (50% mortality)
• Pathogenesis
- NOT fully understood (No ST or LT or CFA)
- Plasmid-borne (EAF, enterotoxin adhesive factor) Bundle-forming Pilus (BFP) -> effacement of MV
• Management: Rehydration therapy

25
Q

Vibrio cholerae

A

• Family Vibrionaceae. Curved Gram-ve rods, (May be linked end to end) forming S shapes. Motile (single polar flagellum)
– Non-spore forming. Oxidase +ve. Halotolerant
– O & H antigens. Serogroup: O1 & O139
– Ferment sucrose & mannose NOT arabinose – Acid sensitive - think about intake.
CHOLERA TOXIN. Bacteriophage encoded. AB toxin. Receptor: Ganglioside GM1

Sx: hypovolemic shock, acidosis, vomiting, rice water stool, mm cramping (d/t dehydration)

Tx: Replace ionic loss. Oral and/or IV admin glucose.
Prevention: Parentally administered vaccine. (killed Vibrio cells) Lasts 3-6 months. Only effective O1 serotype
Not Recommended by FDA. Sanitation & Hygiene.

Dx: Clinical presentation, screening of stool samples -> oxidase activity. Sucrose +! vs other Vibrio.
Cholera Ags: Serotypes: Inaba, Ogawa, and Hikojima. Biotypes: “classic” and El Tor

26
Q

Clostridium perfringens

A

2 different dz’s
1) Necrotic enteritis (Darmbrand & Pig-Bel)
RARE (Papua New Guinea) C. perfringens strain type C

2) Type A food-borne infection
Major cause food-borne infection in U.S
C. perfringens strain type A

  • Sources of C.perfringens type A. Ubiquitous: soil/dust. 50% raw/frozen meat contain C. perfringens. Intestinal tract Humans & Domestic animals
  • If nml flora of animals, sporulate during cooking, germinate when food is cooling. When in GIT, make C. perfringens enterotoxin (CPE) -> alters SI permeability
  • Sx’s: watery diarrhoea & severe abdominal pain. NO FEVER, NAUSEA, AND VOMITING.
  • Mortality rate = 0. Elderly & Immunocompromised patients (monitored)

Dx
• Case hx and sx’s
• Large # (>10^6/g) C. perfringens spores in faeces
• Large # vegetative cells (same serotype) in incriminated food (>10^6/g)
• Presence of enterotoxin in feces

27
Q

Bacillus cereus

A

Diarrheal -> Resembles C. perfringens. Characterization: diarrhoea & abdominal pain. Incubation: 8-16hrs. Duration: 12-24 hr.
(Foods: meat & vegetable dishes, sauces, pasta, desserts & dairy products)

LT Enterotoxin(s) prodn vegetative growth (late exponential phase) (in SI) adenyl acyclase-cAMP

Vs. food poisoning, infxn has: longer incubation, ENTEROTOXIN, water diarrhea (instead of vomiting), LT protein (vs ST neurotoxin)

28
Q

Rotavirus

A

Family Reoviridae. Wheel-shape, non-enveloped
• 10 human rotavirus serotypes (G1-G4 important) Group A(1): Worldwide distribution. Non-group A (B(2),C(3)): Limited distribution (B - China)
• 80% of children have had it by age 4 or 5
• Factors for High Incidence & Mort: Unsafe water, inadeq sanitation
Age: 5 years ASX. Protection against diarrhoeal infection
• Temperate, Developed countries: “Winter Gastro”
Tropical, Developing countries: Year long (Summer)
• Transmission: vary Faecal-oral route, water-borne, or air-borne
• Incubation period:<48hrs(1-3days)
• Replication: epi cells of SI
• Shedding MAY persist for 10 days or more. Peak within 8 days

29
Q

Rotavirus clinical info

A

• Histopath studies: shortening & blunting of villi patchy, irregular intact mucosa,
mononuclear cell infilt of LP
• Diarrhea d/t loss of absorptive area and flux of H2O/fluid across dmged surface

  • Illness: Sudden onset waterydiarrhoea +/- vomiting. Up to 6 days (longer: immunocompromised)
  • Complications: Dehydration, severe & LIFE-THREATENING

Detection
• Virus in stool (peak at day 3/4 of diarrhea)
• Latex agglutination
• ELISA/EIA (for characterisation)
• Electron Microscopy (labour intensive, insensitive)
• Electrophoresis of RNA segments

30
Q

Rotavirus vaccines

A

1st Rotavirus Vaccine (Rotashield®)
• 1998: FDA approved
Live Oral Tetravalent Vaccine: 3 x 2.5ml doses @ 2, 4 & 6 months of age
• Prelicensure Studies: Prevent 50% rotavirus cases, 70% severe cases; 100% associated dehydration
• Adverse rxns: Intussusception 15 cases
• July 1999: CDC recommended discontinuing use. FDA notified manufacturer & doctors

• Merck: RotaTeq®
– Live, oral, pentavalent (G1, G2, G3, (G4), P7 and P1
– 1st dose between 6-12 weeks of age
• 3 doses: 6-32 weeks of age
– 3rd dose NOT given after 32 weeks of age
• FDA Approved: Feb 2006

• Glaxo_Smith_Kline:Rotarix®
• Live, attenuated oral, GP1
• 2doses
– 1st 2 months of age – 2nd 4 months of age
• FDA approved License April 2008
Suspended in March 2010 for about 1 mo d/t – Porcine Circovirus 1 & 2 (PCV1; PCV2) DNA found

31
Q

Norwalk virus (Norovirus)

A

• Originally Family Calciviridae (2002, Noroviridae)
• 4 Genera (Norovirus, Sapovirus, Lagovirus & Vesivirus)
Non-enveloped
Amorphous surface: feathery, ragged outline
Virion: ss +ve sense RNA (7.5kb)

• CRUISE SHIPS
• Estimated 50% outbreaks of acute, nonbacterial gastroenteritis (US)
• Older children & adults (Children < 5 yrs) (Camps, schools, nursing homes, etc.)
• Winter seasonality?
– Winter Vomiting Disease

32
Q

Norwalk-like viruses

A 
• Location of outbreak
Ohio, Hawaii, Snow Mountain, Colorado 
Taunton & Southampton (UK)
Otofuke & Sapporo (Japan)
• Considerable genetic homology with Norwalk
• Shared virological characteristics
33
Q

Sapoviruses

A

• Family Calciviridae
• Children & Adults (Elderly)
5 genogroups (GI-GV), Humans I II IV & V
66% gastroenteritis outbreaks in Long term Care facilities (LTCF’s)

34
Q

Norwalk virus (Norovirus) pathogenesis

A

• Transmission: 1ary Faecal-oral route Water-borne
Food-borne (raw shellfish)
• Virus multiplies in small intestine
• Produces transient lesions of intestinal mucosa
• Spares large intestine (NO faecal leukocytes)
• Shed in faeces

• Mild & Brief: 24-48 hr following ingestion Lasts 24-60hrs
Characterised: abdominal cramps, myalgias, malaise, headache, nausea, low grade fever & 1-2 days diarrhoea
• Fatalities are RARE

• Diagnosis Criteria (Epidemiological)
– 1) Mean (or median) illness duration of 12-60 hrs
– 2) Mean (or median) incubation period of 24-48 hrs – 3) > 50% of people with vomiting
– 4) No bacterial agent previously found
• Disadvantage: NOT SENSITIVE

  • Virusinstool(peakatday2/5afteronset) • Difficult to culture
  • RT-qPCR assays
  • High Sensitivity (10-100 virus copies/reaction)
  • RT-PCR (for genotyping) • EIA(notsensitive)
35
Q

Norovirus Vaccine

A

• LigoCyte®PharmaceuticalsInc.
– norovirus virus like particle (VLP) vaccine (+ chitosan &
monophosphoryl lipid A adjuvants)
• 2 doses: 3 weeks apart – IM
• Clinical trials: 47% efficacy against illness – Illness less severe, shorter duration
– No observed side effects

36
Q

Adenoviruses

A

• FamilyAdenoviridae
• 2 Genera: Mastadenovirses & Aviadenoviruses
Icosahedral protein shell
252 capsomeres
Protein core: ds DNA
12 vertices PENTONS each with fibre
2 serotypes associated: 40 & 41 (Group F)

• Main Target: Respiratory Tract
• Infect: Epithelial cells of Pharynx, Conjunctiva, Small
Intestine & occasionally other organ systems
• Spread beyond regional lymph nodes NOT usual
• Many replicate in intestine & present in stool
• Diarrhoea with or without vomiting
• 5-15%casesdiarrhoea(2oRotavirus)

37
Q

Astroviruses

A
  • Family Astroviridae
  • Non-enveloped
  • Smooth or slightly indented outer shell
  • Inner 5 or 6 pointed star shaped core

• 2-8%sporadiccasesininfants(3oRotavirus)
• Infectionthroughyear:Peakinwinter
• 7 human serotypes
UK: Type 1 prevalent (65% cases)
Mexico: 6% cases, Type 2 prevalent (31%) Japan: Type 6

38
Q

Toroviruses

A
  • Emerging GI Pathogen (similar to coronavirus (ssRNA))

* At risk?: Aged, immunosuppressed & hospitalised

39
Q

Hepatitis A virus (HAV)

A
  • 27nm icoshedral particle (typical Picornaviridae structure)
  • Non enveloped symmetrical ss(+) RNA
  • Spread: Faecal-Oral route, person-to-person Poor sanitation & overcrowding

Virus shedding in faeces (10-14d after exposure)

40
Q

Hepatitis E Virus (HEV)

A

• Icosahedral particle (similar Calciviruses)
• Non enveloped symmetrical (+) RNA
• Final taxonomic classification?
• 1980: Enterically-transmitted non-A, non-B hepatitis Indian subcontinent
(Russia, SE Asia, N America, Mexico)
• Incubation longer than HAV (mean 6 wks)

41
Q

Inflammatory diarrhea - food associated: foodborne infection

A
  • Ingestion of organisms present in food
  • Colonisation & Invasion of intestines (Except EAEC & EHEC)
  • Symptomology: Bloody diarrhoea (May begin as watery diarrhoea). Longer incubation due to colonisation. Fever may be present
  • Toxins Affect: Enterotoxins &/or Cytotoxins
42
Q

Shigella sp.

A

• Shigella sp.
Genus: 50 species, into 4 groups “O” antigens
GROUP A: Shigella dysenteriae - most severe
GROUP B: Shigella flexneri
GROUP C: Shigella boydii
GROUP D: Shigella sonnei - least severe
Closely related to E. coli (antigens & toxin-capabilities))

  • Endotoxin(Oantigen)
  • Exotoxin:Enterotoxin acts as neurotoxin. Causes: meningismus & coma, ulceration
  • NAD glycohydrolase: Destroys all NAD in human cells. Shuts down metabolism. Cell death
  • Invade epi cells of LI -> plasmid-encoded endocytosis ->
    membrane ruffling, production of invasins
  • Shigella multiply and spread to adjacent epithelial cells
43
Q

Bacillary Dysentery

A
  • Shigella dysenteriae type 1 (Shigabacillus)
  • Shiga toxin (cytotoxin) - inhibits protein synthesis

Acts as:
Enterotoxin - produces diarrhea
Exotoxin - inhibits sugar & Aa absorption in SI Neurotoxin - affects CNS

44
Q

Shigellosis by other Shigella sp.

A

• Shigella sonnei - children <5 years (day-care)
• Shigella flexneri – men who have sex with men
• Shigella boydii - rare
Readily transmitted faecal-oral route: Sanitation breaks down (4 F’s)
• Bloodstream invasion RARE

Diagnosis, Isolation & Identification
• Isolation from stools, water & food
Non-motilem Gram-ve rod
NO fermentation lactose
NO utilization citric acid
NO H2S production (except. S. flexneri) NO gas from glucose
45
Q

ENTEROINVASIVE E. coli (EIEC)

A

SE Asia/S America
Similar to Shigellosis less severe (Often mistaken) NO Shiga toxin
Infective dose as few as 10 organisms
• Pathogenesis
Invasion of enterocytes in LARGE INTESTINE Inhibits protein synthesis, killing host cells
Causes dead WBC’s (pus), RBC’s and mucosal cells in stool
• Management Rehydration therapy

46
Q

S. Typhi

A
  • Enteric Fever
  • Important morbidity/mortality worldwide
  • US: ONLY seen in traveller’s to Asia, Mexico, India TYPHOID FEVER
    • Enteric fever: S.Paratyphi A,B or C
  • ASYMPTOMATIC CARRIAGE. Carrier state important in transmission
Motile, Gram-ve rod
NO fermentation lactose
H2S production
Gas from glucose 
Serotyping

Diagnosis of S. Typhi 1) History of travel to endemic areas

2) Rose coloured spots on abdomen (2-4days)
3) Examination of blood (anaemia, leukopenia, absence of eosinophils)
4) Isolation of S. Typhi on S-S agar
5) Positive Widal reaction (agglutination of O & H antigens)

47
Q

Campylobacter spp

A 
# 1 Food-borne bacterial disease in the West
From ingested contaminated liquid or solid food, i.e., unpasteurized milk, raw/partially cooked poultry & contaminated
water

Small, curved-spiral rods, Gram -ve, Non-sporing, Motile (single polar flagellum).
Microaerophilic - req. 5% O2, 10% CO2 for growth
DO NOT ferment CH2O
Catalase +ve
No growth at 25C, but at 37C, readily 42 - 43C

• Intestinal tract of wide variety of wild & domestic animals (Zoonotic)
- Commercially raised poultry 
- Normal commensal of cows 
- Long-term commensal of sheep 
- Pigs (carriers of C. coli)
- C. jejuni intestinal commensal 
- Cats & dogs
• Faecal contaminated water
• Dose - 104 org (as few as 500 cells)
INVASION:
• Inflam & Bacteremia suggest invasion
TOXIN:
– Endotoxin
– Enterotoxin: watery diarrhoea
– Cytotoxin: Verotoxin similar to Shiga toxin: (Haem colitis) Significance not understood
48
Q

Campylobacter clinical and dx

A

• Symptoms appear 3-5 days after ingestion Vomiting - slight
Diarrhea - often profuse (green?) Abdominal pain - often severe
Prostration - often severe
Pyrexia - often present
Other symptoms - bloodstained faeces

• Management
Usually self-limiting
Erythromycin - eradicate C. jejuni from faeces
Severe abdominal pain - aminoglycoside, chloramphenicol, doxycycline
• Association/Complications
– Reactive arthritis (1% cases): Knee joint (6-12 mnths) – Acute Inflammatory Demyelinating Polyneuropathy:
Guillain-Barré syndrome (GBS) (30% cases) AKA: Acute Motor Axonal Neuropathy

Def dx: oxidase +, catalase +

49
Q

Yersinia enterocolytica

A

Yersiniosis - lesser cause Y. pseudotuberculosis

  • Common in children <7 yrs (1-4 y); adults
  • Rivals Salmonella - acute gastroenteritis (cooler climates)
  • -1 - +40C (Psychrotroph – Facultative psychrophile

Pathogenesis - poorly understood
• Invasive induces inflammatory response
Distal ileum (gut-associated lymphoid tissue)
Adjacent tissues & mesenteric lymph nodes also infected
(mimic appendicitis)
• (Chromosomal) ST Enterotoxin •

50
Q

Yersenia enterocolytica clinical and dx

A

CLINICAL FEATURES
Self-limiting enterocolitis
Incub period 3-7 days. Lasts 14-21 days (Longer)
Sx’s: abdominal pain & diarrhoea. Mild fever, vomiting rare

Post-infective Reactive Arthritis (Autoimmunity Arthritis)
• Small proportion patients Pathogenesis poorly understood
• MAYBE
– Induced polyclonal T-cell stimulation (toxin)
– Non-specific immune stimulation of invasin binding to b1 integrins on T lymphocyte
– Other bacterial antigens

Special investigation
• Diagnosis from stool is possible
Often considered late: rising antibody titres in paired serum
• MacConkey(pinpoint colonies/48hrs)
• Specialized Yersinia media

51
Q

NON - CHOLERA Vibrio’s

A 
Not agglutinated by anti O1 sera
Halophilic organisms (Common coastal waters)

Vibrio parahaemolyticus
• Ingestion of raw/poorly cooked seafood Acute abdominal pain, vomiting & watery diarrhea
Japan - raw fish (# 1 Food-borne)
US - shellfish

Vibrio vulnificus

  • Diarrhoea & infection of cuts (Salt water abrasions)
  • Virulent strain
  • Intense skin lesions (gastroenteritis & even severe bacteremia)

Dx:
• Clinical presentation (Not Cholera)
• Screening of stool samples. Oxidase activity
Thiosulphate-citrate-bile salts-sucrose (TCBS) agar. Sucrose (differentiating agent)
Sucrose -ve V. parahaemolyticus, V. vulnificus

52
Q

Enteraggregative (EAEC) E. Coli

A

• PATHOGENESIS:
Not fully understood
NO EAF (Enteric Adherence factor)
Possess AAF (Aggregative Adherence factor)
Thought: 3 stages
1) Initial adherence to intestinal mucosa and/or mucus layer (fimbriae)
2) Enhanced mucus prodn -> thick mucous biofilm
3) Cytotoxin prodn? -> Dmg to intestinal cells

causes: LIFE THREATENING CONDITIONS
HAEMORRHAGIC COLITIS
HAEMOLYTIC UREMIC SYNDROME (8 -11% cases)
Acute renal failure
Thrombocytopenia
Microangiopathic haemolytic anaemia
THROMBOTIC THROMBOCYTOPENIA PURPURA
Pathogenesis
Attachment (similar to EPEC)
Phage encoded: CYTOTOXIN - VEROTOXIN
2 types (VT1 & VT2) both AB toxins
Shiga-like toxin (rRNA) blocks protein synthesis
53
Q

Dx of E. coli’s

A

1) MacConkey’s agar (Red-Pink colonies)
2) Sorbitol MacConkey’s agar (no fermentation EHEC)
3) (ETEC) Inoculate mouse adrenal cells: stimulation of adenylate cyclase by LT/ST
4) ELISA on toxin bound to antibody
5) DNA probe to detect toxin genes

54
Q

Clostridium difficile

A

• 2 toxins
Toxin A enterotoxin (fluid accum in bowel)
(weak cytotoxin most mammalian cells)

Toxin B potent cytotoxin
Decreases cellular prot syn & disrupts
microfilament system of cells (similar to diphtheria toxin)

Clinical Symptoms
• Vary: mild diarrhoea -> severe abdominal pain accompanied fever (>101F) & severe wkness
• Diarrhoea: watery,usually non-bloody (5-10% bloody), xs mucus & pus (or blood) Hypoalbumineia & Leukocytosis common

• Dx: Difficult. Not distinguished from UC & Crohns
Colonic examination (presence of pseudomembrane) AND Isolation C. difficile, associated abx therapy
Management
Discontinue abx - sx's resolve 1-14 days
If severe or no response; treat oral abxs: Vancomycin (“gold” standard)
or Metronidazole (milder infections) 
Relapses in 15-20% patients

Dificid (fidaxomicin) bid 10 days. Approved by FDA (2011)

55
Q

Helicobacter pylori

A 
Biological carcinogen
Gram -ve, Non spore-forming, Curved to spiral (1-3 turns).
Motile - polar (5-6) flagella 
Microaerophilic 2-5%O2, 5-10%CO2 
Catalase +ve; Urease +ve 
Coccoidal forms under culture

ASSOCIATED CAUSE
• Gastritis (stomach atrum)
• Duodenal ulcers (& gastric ulcers)
• Gastric cancer

Pathogenesis
Gastric colonisation is common Route of infection UNCLEAR
• Mechs UNDER INVESTIGATION
Role of cytotoxin, urease, mucinase, flagella
• UREASE allow H. pylori survival at pH 2.0
Able to split ammonia from urea = alkaline environment
• Virulence Factors: allowing for adhesion & damage to mucosa
- cagPAI: VacA cytotoxin; BabA; OipA

Jan 28th 2003, FDA approved Helivax Inactivated, whole cell vaccine.

56
Q

Mgmt of diarrheal dz

A

• Oral rehydration (ORT): till normal rehydration restored (determined by: clinical condition/body weight)
Sodium: 150-155mmol/l
Glucose: 200-220mmol/l
Potassium: 4-5mmol/l

  • Intravenous rehydration: shock, exhaustion precluding oral feeding and oral rehydration failure
  • Antiemetic drugs: reduce fluid loss

Term 3/4 Flash Cards (7 decks)

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