3. GIT 2

Question 1

Name some Gram Negative Organisms of the GIT

Answer 1

Salmonella
Shigella
Escherichia coli
Yersinia enterocolitica

Campylobacter Vibrio

Question 2

Name some Gram Positive Organisms of the GIT

Answer 2

Clostridium
Bacillus
Staphyloccocus
Listeria

Question 3

Viruses that infect GIT

Answer 3

Norovirus
Rotavirus
Adenovirus

Question 4

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

Answer 4

Campylobacteriosis

GRAM NEGATIVE, curved, motile, microaerophilic

Question 5

CAMPYLOBACTER spp- epidemiology?

Answer 5

• 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

Question 6

What are the most common CAMPYLOBACTER spp

Answer 6

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

Question 7

What is the clinical presentation of Campylobacteriosis is

Answer 7

• 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

Question 8

What are the complications of Campylobacteriosis

Answer 8

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)

Question 9

How do you diagnose Campylobacter

Answer 9

• 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

Question 10

How do you treat Campylobactor?

Answer 10

• 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

Question 11

VIBRIO SPECIES- microbiology?

Answer 11

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

Question 12

Epidemiology of Vibrio!

Answer 12

• 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.

Question 13

What is the pathophysiology of Vibrio Cholera

Answer 13

• 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)

Question 14

What are the clinical manifestations of Vibrio spp?

Answer 14

• 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

Question 15

What are the clinical manifestations of VIBRIO PARAHAEMOLYTICUS?

Answer 15

• 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

Question 16

What is the diagnostic strategy for Vibrio spp?

Answer 16

• 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

Question 17

What are the treatment strategies for Vibrio Spp?

Answer 17

• 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

Question 18

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

Answer 18

Clostridium Difficile- colitis

Clostridium Perfringens- Gas Gangrene, food poisoning, enterising necroticans

Question 19

Microbology of Clostridium Difficile?

Answer 19

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

Question 20

Epidemiology of Clostridium Difficile?

Answer 20

•	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

Question 21

Risk factors for C.difficile associated disease

Answer 21

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

Question 22

Clinical Presentation of Clostridium Difficile

Answer 22

• 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

Question 23

What should your differential consider with clostridium difficile?

Answer 23

• 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

Question 24

What are the diagnostic strategies for C.difficile?

Answer 24

•	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

Question 25

What are the treatment strategies for C.difficile?

Answer 25

• 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?

Question 26

What is the epidemilogy of Clostridium perfringens?

Answer 26

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

Question 27

What are the biotypes of C.perfringens?

Answer 27

``` 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 ```

Question 28

What is the clinical presentation of Clostridium perfringens?

Answer 28

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

Question 29

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

Answer 29

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

Question 30

What are the clinical manifestations of clostridium perfringens type a?

Answer 30

* 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

Question 31

What are the complications of clostridium perfringens?

Answer 31

• 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%

Question 32

What are the treatment strategies of C.perfringens

Answer 32

• 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

Question 33

What is the microbiology of LISTERIA MONOCYTOGENES

Answer 33

* 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

Question 34

What is the epidemiology of LISTERIA MONOCYTOGENES

Answer 34

• 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)

Question 35

What are the clinical manifestations caused by Listeria Monocytogenes?

Answer 35

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

Question 36

What does Listeria induced gastroenteritis present as?

Answer 36

• 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

Question 37

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

Answer 37

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

Question 38

What does listeria induced granulomatosis infantisepticum present as?

Answer 38

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

Question 39

What does neonatal meningitis oresent like? (listeria induced)

Answer 39

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.

Question 40

How do you diagnose Listeria

Answer 40

* Gram stain of CSF | * Culture from blood and CSF on selective medium with cold enrichment

Question 41

How do you treat listeria?

Answer 41

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)

Question 42

What is the microbiology of Bacillus Cereus?

Answer 42

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

Question 43

What is the epidemiology of B. cereus

Answer 43

• 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

Question 44

How does Bacillus Cereus present?

Answer 44

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

Question 45

What are the treatment strategies for bacillus cereus

Answer 45

* 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)

Question 46

What is the epidemiology of STAPHYLOCOCCUS AUREUS

Answer 46

``` 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 ```

Question 47

What is the pathogenesis of staph aureus

Answer 47

* 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.

Question 48

What does staph aureus present as?

Answer 48

• 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)

Question 49

What are the treatment strategies for staph aureus?

Answer 49

• 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