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Microbiology CAM202 > 3. GIT 2 > Flashcards

3. GIT 2 Flashcards

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1
Q

Name some Gram Negative Organisms of the GIT

A

Salmonella
Shigella
Escherichia coli
Yersinia enterocolitica

Campylobacter Vibrio

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2
Q

Name some Gram Positive Organisms of the GIT

A

Clostridium
Bacillus
Staphyloccocus
Listeria

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3
Q

Viruses that infect GIT

A

Norovirus
Rotavirus
Adenovirus

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4
Q

CAMPYLOBACTER spp cause what disease? what is the microbiology of this organism?

A

Campylobacteriosis

GRAM NEGATIVE, curved, motile, microaerophilic

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5
Q

CAMPYLOBACTER spp- epidemiology?

A

• All ages affected BUT most cases occur in
o Children <5 years of age
o Individuals between the ages of 20 and 29 years “Backpackers diarhhoea”
o Opportunistic infection in patients with AIDS
• Zoonotic: most infections acquired by consuming infected:
o Raw or undercooked poultry meat
o Beef, pork
o Milk
o Untreated water
• Further sources for infection- handling infected pets and farm animals

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6
Q

What are the most common CAMPYLOBACTER spp

A

Most common species isolated
• Campylobacter jejuni
• C. coli
• C. fetus
• C. cinaedi and C.fennelliae (sexually transmissible)
Attaches to the mucosal surfaces of the jejunum, ileum and colon. Disruption of the epithelial cells

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7
Q

What is the clinical presentation of Campylobacteriosis is

A

• Rapid onset, after 2-5 days of incubation, disease onset is rapid with:
o Fever
o Cramping abdominal pain
• Diarrhoea onset lags (24 to 48 hours)
o Typically stools are loose, bile coloured, then become watery
o Eventually become grossly bloody (or occult blood present in stools (inflammatory diarrhoea)
o Can persist for weeks
• Constitutonal symptoms are the rule and include
o Malaise
o Myalgia
o Headache
o Vomitting
o Backache
o Arthralgias

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8
Q

What are the complications of Campylobacteriosis

A 
Complications are generally rare but can include:
•	Septicaemia
•	Endocarditis
•	Osteomyelitis
•	Cholecystitis
•	Pancreatitis
•	Meningitis
•	Septic thrombophlebitis
•	Reactive Arthritis
•	Guillain- Barre Syndrome (usually presents a few weeks after diarrhoeal illness)
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9
Q

How do you diagnose Campylobacter

A

• Culture from stool sample
o Selective medium containing blood or charcoal (modified charcoal, cefoperazone, desoxycholate agar (mCCDA; Preston agar)
o Incubation under microaerophilic atmosphere (5% 02, 10% CO2) for 48-72 hours
o Test for oxidase and catalase positive phenotype
• Stool antigen testing

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10
Q

How do you treat Campylobactor?

A

• Self limited
• Supportive rehydration therapy
• No clinical improvement, or worsening condition consider
o For diarrhoea
• Erythromycin or azithromycin; tetracycline* (amoxicillin/clavulanic acid in young children)
o For systemic infections
• Aminoglycoside, chloramphenicol, or imipenem

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11
Q

VIBRIO SPECIES- microbiology?

A
  • Highly motile, Gram-negative, curved or comma-shaped rods with a single polar flagellum
  • Prototype of an enterotixic bacterium that causes secretory (watery) diarrhea
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12
Q

Epidemiology of Vibrio!

A

• Serotypes able to cause disease in humans
o Vibrio cholera 01 which is divided further into two biotypes: cholera and eltor
• Example, written as V.Cholerae biotype EI Tor
o Virbrio Cholerae 0139 Bengal (so-called non-01 strain)

• Other Vibrio species able to cause disease in humans
o Vibrio parahaemolyticus and Vibrio vulnificus

  • Cholera is a nationally notifiable disease
  • Most Vibrio species grow well in naturally water environments (estuaries, coastal seawaters)

• Cholera and Vibrio outbreaks are associated with faecal-contaminated water (ie. faecal-oral transmission) or raw/inadequately prepared seafood harbouring bacteria (crabs, oysters, mussels, shrimp, lobsters). But also in some cases:
o Imported seafood
o Cooked rice
o Frozen or fresh coconut milk
• Asymptomatic individuals infected with cholera can also be a reservoir, especially in areas where cholera is endemic.

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13
Q

What is the pathophysiology of Vibrio Cholera

A
  • The A/B cholera toxin (-84KDa) binds the GM1 ganglioside receptor on the intestinal epithelial cell via the B subunit.
  • Binding followed by endocytosis of the A subunit of the A/B toxin
  • The A subunit is subsequently cleaved into enzymatically active “A1” subunit
  • A1 subunit stimulates expression of adenylate cyclase (AC) and cAMP production
  • cAMP, in turn, induces expression of the cystic fibrosis transmembrane conductance regulator (CFTR) resulting in ion and water efflux into intestinal lumen (hence secretory diarrhoea)
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14
Q

What are the clinical manifestations of Vibrio spp?

A

• After 24-48 hours of ingesting contaminated seafood, classic epidemic cholera presents with:
o Copious amounts of “rice water” diarrhoea
o Abdominal cramps
o Nausea
o Vomiting
o A low grade fever, occassionaly
• In severe cases, fluid loss can be as much as 1 litre per hour, some patients lose enough water to warrant hospitalization (ie. hypovolemic shock), and fatality rates can be as high as 25-50% in untreated population
• Average duration of illness is 7 days

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15
Q

What are the clinical manifestations of VIBRIO PARAHAEMOLYTICUS?

A
  • Symptoms usually manifest after 8-12 hours (but can range from 4-48 hours) after ingesting contaminated foods
  • Explosive watery diarrhea, but volumes lost lower than with cholerae

• Headache
• Nausea
• Vomiting
• Low grade fever
• Infections also manifest as serious wound infections* (from contaminated waters)
• Septicaemia*
o *patients with underlying disease, liver disease, diabetes mellitus, alcoholism

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16
Q

What is the diagnostic strategy for Vibrio spp?

A

• Specimens should be collected (from stool or rectal swab) early and transported for inoculation on culture media promptly
o Sensitive to acid pH (grow better at alkaline pH 9-9.6)
o Horse Blood Agar (HBA)
o MacConkey Agar
o Thiosulfate citrate bile salts sucrose (TCBS) agar
o Enrichment broths (alkaline peptone broth)
• Serotyping withy polyvalent antisera (O grouping antisera)
• Very fragile bacteria and die quickly

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17
Q

What are the treatment strategies for Vibrio Spp?

A

• For Classic Cholera
o Oral or IV fluid hydration (as dictated by the clinical picture)
o Severity and duration of disease has been shown to be reduced with antibiotic therapies
• Azithromycin, doxycycline (amoxicillin in children/pregnant women)

• For Vibrio parahaemalyticus & Vibrio vulnificus
o Rehydration for patients with severe infections ; plus
o Wounds: doxycycline (amoxicillin in children/pregnant women)
o Sepsis: gentamicin

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18
Q

What are the two different Clostridium species (that occur in GIT?)

A

Clostridium Difficile- colitis

Clostridium Perfringens- Gas Gangrene, food poisoning, enterising necroticans

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19
Q

Microbology of Clostridium Difficile?

A

• Anaerobic spore-forming Gram +ve bacillus; normally found in the colon

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20
Q

Epidemiology of Clostridium Difficile?

A 
•	Associated with
o	Asymptomatic colonization- not very adaptable, normally outcompeted by normal flora
o	Severe diarrhoea
o	Pseudomembranous colitis (possibly associated with toxic megacolon and intestinal perforation)
•	C. difficile is a unique because it causes diarrhea primarily during or after oral or intravenous antibiotic administration, examples:
•	Quinolones
•	Clindamycin, Lincomycin
•	Penicillin, Ampicillin 
•	Cephalosporins
•	Tetracycline
•	Chloramphenicol
•	Erythromycin
21
Q

Risk factors for C.difficile associated disease

A
  • Age >65
  • Underlying illness
  • Nasogastric intubation
  • Use of antiulcer medications
  • Extended hospital stay
  • Long-term care facilities
22
Q

Clinical Presentation of Clostridium Difficile

A

• Symptoms may appear during the course of antimicrobial therapy or else, more commonly, 3 to 4 weeks after discontinuation. Manifests more like an invasive diarrhoea rather than toxigenic

Young children have more severe symptoms than adults: o	Fever o	Nausea o	Severe cramping of the lower abdomen o	Distension o	Profuse watery stools o	Occult blood; faecal leukocytes (but hemetaochezia is uncommon) o	Mortality rate is increased when pseudomembranous colitis is present
23
Q

What should your differential consider with clostridium difficile?

A

• 10% of all patients (Especially children) treated with antibiotics develop diarrhoea not associated with C. difficile
o Mild watery diarrhoea with no cytopathic toxin induced colitis

24
Q

What are the diagnostic strategies for C.difficile?

A 
•	Diagnoses confirmed when toxins are detected in the stool sample in the presence of associated enteritis
•	Use of stool toxin detection assays:
o	EIA (toxin A/B)
o	PCR (toxin A/B gene)
*Toxin A = enterotoxin
* Toxin B= cytotoxin
25
Q

What are the treatment strategies for C.difficile?

A

• Resolution usually occurs within 48 to 72 hours after antibiotic therapy stopped
o If diarrhoea is not resolved, or if severe
• Metronidazole (orally/intravenous)
• Vancomycin (orally)
• Clinical improvement usually follows within 36 to 72 hours
• Diarrhoea resolves over a period of 5 to 7 days BUT stool samples can still show presence of toxins for weeks
• Patients can relapse (25%)
• Probiotics? Saccharomyces boulardii + antibiotic treatment
• Faecal transplant?

26
Q

What is the epidemilogy of Clostridium perfringens?

A

• Ubiquitous organism, found in:
o Soil
o Water
o Intestinal tracts and faeces of human and animals

27
Q

What are the biotypes of C.perfringens?

A 
Biotypes of C.perfringens	Toxin Produced
Type A*- breaks down platelets, RBC	Alpha
Type B	Alpha, beta, epsilon
Type C*	Alpha, beta
Type E  & Type D	Alpha, Iota
All biotypes produce an enterotoxin
•	**= produce disease in humans
28
Q

What is the clinical presentation of Clostridium perfringens?

A

Soft Tissue infections
• Cellulitis
• Supportive myositis
• Myonecrosis (gas gangrene)
Gastroenteritis
• Food-borne illness (C.perfringens Type A)
• Necrotising enteritis (C.perfringens Type C)

29
Q

Explain the pathophysiology of C.perfringens Type A (food-borne illness)

A

Released CPE toxin binds to ileum and jejunum epithelial cells, (rarely in the duodenum), resulting in loss of fluids and ions.

30
Q

What are the clinical manifestations of clostridium perfringens type a?

A
  • Illness caused by the enterotoxin produced during sporulation
  • Symptoms and signs usually occur within 6 to 24 hours after ingestion of contaminated food
  • Acute onset of abdominal cramps (fever, nausea, vomiting usually absent)
  • Frequen passage of watery diarrheal stools
  • Self-limited, rarely lasts more than 24 hours
31
Q

What are the complications of clostridium perfringens?

A

• Enteritis necroticans (also known as “pig-bel”)
o Common in Melanesian Islands (Papua New Guinea, Vanuatu, Soloman Islands)
o Occurs after ingestion of food heavily contaminated with C.perfringens type C strain (beta toxin producing strain)
o Acute onset of severe abdominal pain, vomiting
o Bloody diarrhoea
o Prostration
o Peritonitis, and shock
o Postmortem reveals diffuse, hemorrhagic, necrotizing enteritis of the jejunum, ileum, and colon
o Mortality of patients approaches 50%

32
Q

What are the treatment strategies of C.perfringens

A

• Dependent on clinical syndrome
• Soft Tissue Infections
o Immediate and aggressive surgical debridement, plus high dose penicillin therapy
o IV benzylpenicillin + metronidazole +/- other antibiotics (eg. Clindamycin)
o Hyperbaric oxygen?
o Prognosis of these patients is poor (40-100% mortality)
o Anti (alpha) toxin no longer available
• Food Borne Illness (C.perfringens Type A)
o Self limited
o Antibiotic therapy is generally not necessary

33
Q

What is the microbiology of LISTERIA MONOCYTOGENES

A
  • Small gram positive facultative anaerobic rods, often arranged in pairs or short chains (can be mistaken for streptococcus pneumoniae or corynebacteria)
  • Exhibits growth over a wide range of temperatures 1-45 degrees. It is beta-haemolytic, and exhibits characteristic tumbling motility under light microscopy
  • Organism is ubiquitous, so exposure leading to transient colonization is a likely event
34
Q

What is the epidemiology of LISTERIA MONOCYTOGENES

A

• Focal epidemics and sporadic cases of listerosis have been associated with ingestion of contaminated
o Undercooked meat and poultry; smoked salmon
o Milk
o Soft cheese
o Unwashed raw vegetables
• Nationally Notifiable Disease
• Establishes as an intracellular pathogen
• Most cases of listeriosis develop in
o Elderly individuals*
o Newborns
o Pregnant women*
o Patients with defects in cellular immunity*
o (in the setting of transplants, lymphomas, AIDS)

35
Q

What are the clinical manifestations caused by Listeria Monocytogenes?

A

Listeria induced gastroenteritis
Infections during pregnancy and neonatal disease (early and late onset)
Granulomatosis Infantisepticum
Neonatal meningitis

36
Q

What does Listeria induced gastroenteritis present as?

A

• Typically non invasive food-borne diarrheal disease
• The median incubation period is 1-2 days, after which time infected person presents with:
o Fever
o Myalgias
o Secretory diarrhoea lasting anywhere from 1-3 days

37
Q

What does listeria induced infections during pregnancy and neonatal disease present as?

A

Infections during pregnancy and neonatal disease (early and late onset)
• Women infected during pregnancy (3rd trimester) can develop bacteremia which can be mild and self limited. Often exhibit signs of:
o Fever, myalgias, arthralgias, back pain and headache

38
Q

What does listeria induced granulomatosis infantisepticum present as?

A

Granulomatosis Infantisepticum
• Early onset sepsis
• Listeria acquired in utero via transplacental transmission
• Can result in premature birth of infected infant; abortion
• Bacteria disseminate, and can be isolated from multiple sites, including the placenta, spleen, liver and skin

39
Q

What does neonatal meningitis oresent like? (listeria induced)

A

Neonatal meningitis
• Late onset (2-3 weeks after birth)
• Bacteria usually acquired via vaginal transmission
• Differential diagnoses should exclude group B streptococcal infection
• Infected adults, particularly immunocompromised, or those with comorbidities can develop meningitis, and infection exhibits a high mortality rate.

40
Q

How do you diagnose Listeria

A
  • Gram stain of CSF

* Culture from blood and CSF on selective medium with cold enrichment

41
Q

How do you treat listeria?

A

Treatment
• Listeria are intrinsically resistant to all cephalosporins, resistance to macrolides and tretracyclines has been observed
• Consider gentamicin with either penicillin or ampicillin (if sensitive to beta lactams, consider cotrimoxazole)

42
Q

What is the microbiology of Bacillus Cereus?

A

• B.cereus is an aerobic, spore forming, Gram positive rod, commonly isolated from soil environments

43
Q

What is the epidemiology of B. cereus

A

• Can contaminate a range of food-products because it tolerates extremes of temperature
o Agricultural products (fruits, grains etc)
o Pastas
o Rice*- the boiling of the rice allows the spores to accumulate, the cooling allows the spores to germinate
o Dairy (pasteurized) and dried milk products
o Dried foods
o Meat
o Chicken
o Vegetables
o Seafood

44
Q

How does Bacillus Cereus present?

A

B.cereus causes two distinct clinical syndromes

Emetic syndrome: caused by a heat stable enterotoxin (bacteria don’t need to be present). After an incubation of 1 to 5 hours
o Profound vomiting
o Abdominal cramps
o Illness is short lived (usually less than 10 hours)
o Recovery is uneventful

Diarrhoeal syndrome: ingestion of the toxin itself, caused by heat labile enterotoxin. Usually after an incubation period of 6 to 14 hours
o Abdominal cramping
o Secretory diarrhea
o Illness duration is usually 12 to 36 hours

45
Q

What are the treatment strategies for bacillus cereus

A
  • Both the emetic and diarrhoeal syndromes are self limiting
  • Antibiotics are not indicated (illness mediated by enterotoxins)
  • Supportive therapy
  • Antiemetic agents can provide effective relief in patients presenting with violent vomiting (consider: Maxolon, sternetil)
46
Q

What is the epidemiology of STAPHYLOCOCCUS AUREUS

A 
Epidemiology
•	People can shed into food, illness usually results when an enterotoxin producing stain of staphylococcus is present in contaminated food before its ingestion
•	Family of enterotoxins, A-E
•	Sources of food stuffs supporting the growth of Staphyloccoci usually includes:
o	Ham
o	Eggs
o	Custard filled pastries
o	Mayonnaise
o	Potato salads
•	Large outbreaks are common worldwide and particularly occur in 
o	School/hospital cafeterias
o	Military bases
o	Airlines
o	Restaurants
47
Q

What is the pathogenesis of staph aureus

A
  • Organism is killed by high temperatures but the staphylococcal enterotoxin is heat stable
  • Toxin does not seem to produce a local effect on the digestive tract
  • Toxin over-stimulates the proliferation of T lymphocytes and leads ot the release of various cytokines
  • Gastrointestinal effects are assumed to result from the release of histamines and leukotrienes from mast cells.
48
Q

What does staph aureus present as?

A

• Rapid onset, beginning 1-6 hours after ingestion of contaminated food
• Affected individuals usually demonstrate
o Fever
o Cramping abdominal pain
o Violent, repeated, retching and vomiting
o Secretory diarrhea- usually mild
o Symptoms are usually short lived (6 to 8 hours)

49
Q

What are the treatment strategies for staph aureus?

A

• Rapid, uncomplicated, spontaneous recovery is the rule
• Antiemetic agents in the presence of dehydration and ongoing vomiting
• Emetic and hydration therapies recommended for
o Infants and children
o Elderly
o Patients with comorbidities

Microbiology CAM202 (1 decks)

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