Gastro-Intestinal Bacterial Infections Flashcards

Describe characteristics of the causative agents (including virulence properties), pathogenesis, clinical features, diagnosis, treatment & prevention of the following:  Shigellosis  Salmonellosis  Typhoid/enteric fever  Non typhoidal Salmonella  Cholera

1
Q

Types of Infectious Bacterial Diarrhoea

A

Salmonella enterica ser Typhi
(Salmonella Typhi)

Salmonella spp.

Shigella sonnei

Shigella boydii

Shigella dysenteriae

Shigella flexneri

Vibrio cholera

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2
Q

Shigella:

Epidemiology

A

Shigella species are closely related to E. coli

Strictly human pathogen, no animal reservoir

Not members of the normal GI microbiota

Transmission: Faecal-oral. Also spread by
food or water contaminated by humans

Outbreaks: Poor personal hygiene standards

  • Very young
  • Very old

All can cause Bacillary dysentery

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3
Q

Microscopy of Shigella

A

Gram-negative bacilli (rods)

Non-motile

Unencapsulated

Facultative

Non-fastidious

Bile-tolerant

Non lactose-fermenter (NLF)

They do not produce H_2S

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4
Q

Types of Shigella

A

Shigella dysenteriae – serogroup A

S. flexneri – serogroup B

S. boydii – serogroup C

S. sonnei – serogroup D

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5
Q

Shigella:

Pathogenesis

A

Highly infectious - very small inoculum required 101
– 102 organisms

Acid-resistant- survives passage through the stomach to reach the intestine

Invasion of the wall of the large bowel - Intense
inflammatory response involving neutrophils and
macrophages

Patches of necrotic epithelium are sloughed and ulcers form

Many strains have been shown to produce an exotoxin -cause secretion of water and electrolytes by cells of the small bowel

Shiga toxin (Stx) that affects both the gut and the
central nervous system

Antibiotic use increases shiga toxin = HUS

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6
Q

Shigella:

Clinical Presentation

A

Initial symptoms appear
approximately 24 to 48 hours after
ingestion of the organisms

Fever, chills, abdominal cramps, and
pain accompanied by tenesmus

Frequent, small-volume, bloody,
mucoid fecal discharge

S. dysenteriae causes dysentery ->severe disease

Infants: convulsions, meningeal
irritation

Transient bacteraemia

Septicaemia rare->immunosuppressed pts

Bacilli in stools-short period

Chronic carriers-recurrent episodes

Do not use Imodium = ↑ toxin absorption

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7
Q

Shigella:

Diagnosis

A
Readily isolated using selective
differential media (eg, Hektoen enteric
agar, XLD agar)

Isolates are identified with further
biochemical tests

Slide agglutination tests using O groupspecific antisera (A, B, C, D) confirm
both the Shigella genus and the
species

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8
Q

Shigella:

Tx

A

Usually self-limiting

Supportive therapy

Treatment reserved for the
immunocompromised, those with
severe/complicated disease as well in
outbreak setting

IV antibiotic Rx + REHYDRATION:

  • Ciprofloxacin
  • Ceftriaxone
  • Azithromycin
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9
Q

Shigella:

Px

A

Standard practices such as
sewage disposal and water
chlorination.

Handwashing and proper
cooking of food, are highly
protective

No vaccines

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10
Q

Salmonella:

Epidemiology

A

1400 serotypes infect humans

2 groups: Humans are the only known source of Salmonella enterica ser Typhi
infections

Typhoid fever caused by:

  • Salmonella enterica ser Typhi
  • Salmonella paratyphi A and B

Typhoid (enteric) fever- severe, higher fatality rate
Paratyphoid fever- less severe, lower fatality rate

Non-typhoid salmonellae (NTS)

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11
Q

Salmonella:

Microscopy

A

Gram-negative bacilli
Motile
All except S. enterica ser Typhi are unencapsulated

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12
Q

Salmonella:

Pathogenesis

A
  1. Ingestion
  2. Small intestine
  3. Macrophage
  4. MLNs-Mesenteric Lymph Nodes
  5. Lymph duct
  6. Transient bacteraemia
  7. Replication in RES»»Septicaemia»>Fever Kidneys Other organs
  8. Gallbladder»»Cholecystitis and Carrier state
  9. Bile to 2
  10. (2.) Inflamation, ulceration: Peyer
  11. Diarrhoea Bleeding Perforation
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13
Q

Salmonella:

Clinical Presentation

A

1) Typhoid (enteric) fever, paratyphoid fever-Caused by S.enterica ser Typhi & S. Paratyphi
2) Acute gastroenteritis, enterocolitis-Caused by non-typhoid salmonellae (NTS)
3) Extra-intestinal infections-Bacteraemia
4) Asymptomatic colonization-carrier state

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14
Q

Typhoid(Enteric) Fever:

Epidemiology

A

NOTIFIABLE MEDICAL CONDITION

S. enterica ser Typhi + S. paratyphi colonise only humans

Transmission: close contact: typhoid fever pt. OR carrier

Infection acquired via ingestion of contaminated food: faecal-oral route

Endemic in developing countries:due to poor socio-economic conditions + sanitation

-SE Asia
-South + Central America
-Africa SALMONELLA:
CLINICAL FEATURES-ENTERIC FEVER

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15
Q

Typhoid/Entreric Fever:

Clinical Presentation

A

Multiorgan infection characterized by prolonged fever, sustained bacteraemia and involvement of MLNs, liver and spleen

Mean incubation period is 13 days

First sign of disease is fever associated with a headache

Fever rises in a stepwise fashion over the next 72 hours and can persists for weeks in untreated patients

A faint rash (rose spots) may appears during the first few days on the abdomen and chest

Many patients are constipated, although perhaps one-third of patients have a mild diarrhea

As the untreated disease progresses, an increasing number of patients complain of diarrhea

Chronic infection of the bloodstream is serious

Effects of endotoxin can lead to myocarditis, encephalopathy, or
intravascular coagulation
Persistent bacteremia can lead to infection at other sites

Biliary tree, with reinfection of the intestinal tract and diarrhea late in the disease

Urinary tract infection and metastatic lesions in bone, joint, liver, and meninges may also occur

Most important complication is hemorrhage from perforations through
the wall of the terminal ileum or proximal colon at the site of necrotic Peyer patches

In patients whose disease has been progressing for 2 weeks or more

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16
Q

Typhoid/Enteric Fever:

DIagnosis

A

Collect BEFORE antibiotic therapy is initiated

Non invasive specimen: Stools

Invasive specimens: Blood Culture, Bone marrow

S. enterica ser Typhi: 90% of pts. have positive BC in first week of illness otherwise positive in the 2nd, 3rd week

Ideally blood and stool cultures should be submitted simultaneously

Bone marrow may remain positive even after 5 days of antibiotics

Urine and stool culture positive in weeks 2 & 3  Specimen culture followed by agglutination with specific antisera including Vi antigen

Serology: Widal->Antibodies against O and H antigens may be suggestive
but not confirmatory. Does not provide information on antibiotic resistance

17
Q

Typhoid/Enteric Fever:

Complications

A

2–5 wks after onset:

Intestinal perforation

Intestinal haemorrhage

Myocarditis

Osteomyelitis

Meningitis, Relapse, Death

10% mortality if untreated

Relapse in 10% of pts.

Carriers: NB source-permanent,
asymptomatic

18
Q

Typhoid/Enteric Fever:

Treatment

A

Positive BC:

  • Ceftriaxone
  • Ciprofloxacin

Empiric Rx:

  • Ciprofloxacin
  • Ceftriaxone
  • Cefotaxime

Carriers:

  • Ciprofloxacin
  • Ceftriaxone
19
Q

Non Typhoid Fever

A

Gastroenteritis»contaminated food

Animal origin

  • Poultry
  • Meat
  • Eggs
  • Dairy products

Proper cooking necessary

Outbreaks occur – common source

GIT infection - does not need antibiotics

20
Q

Non-Typhoid Salmonella Gastroenteritis/Enterocolitis:

Clinical Presentation

A

S. enteritidis

Acute salmonella gastroenteritis: mild to severe

Most cases are self-limiting

Symptoms may appear 8 to 36 hours after ingestion of contaminated food

Nausea, vomiting, fever, and chills, accompanied by watery diarrhea and abdominal pain

Sometimes bacteraemia, bacteriuria, occult abscess

The infection may be more severe in very young children, elderly adults, and
patients with other underlying disease

Dissemination occasionally occur and in such cases, antimicrobial therapy is required

21
Q

Non-Typhoid Salmonella Gastroenteritis/Enterocolitis:

Lab Diagnosis

A

Depends on culture and ID of organism from stools

22
Q

Non-Typhoid Salmonella Gastroenteritis/Enterocolitis:

Treatment

A

Severe illness-extreme of ages

Patient septic and/or sick enough to be
hospitalized

Immune compromised

Sick enough to hospitalize

HIV & sickle cell anaemia is a risk factor for invasive
infections

Empiric treatment if
indicated:
-Ciprofloxacin
-Ceftriaxone
-Cefotaxime
23
Q

Non-Typhoid Salmonella Gastroenteritis/Enterocolitis:

Prevention

A

Sanitation + hygiene

Cook food thoroughly

Carriers: do not handle or prepare food

Vaccination (travelers) only for S typhi protection moderate not absolute

24
Q

Salmonella:

Bacteremia

A

Can be with or without extraintestinal foci of infection

Characterized primarily by prolonged fever and intermittent bacteremia

Serotypes most commonly associated with bacteremia are S. enterica ser Typhi, Paratyphi, and Choleraesuis

Young children may experience fever and gastroenteritis with brief episodes of bacteremia

Adults, may experience transient bacteremia during episodes of gastroenteritis or develop symptoms of septicemia without gastroenteritis

The risk of metastatic complications could be more severe than the bacteremia itself, even in individuals who do not have underlying diseases

Cases of septic arthritis can also occur in patients who had asymptomatic salmonellosis

25
Q

Salmonella: Carrier State

A

Individuals who recover from infection may harbor the organisms in the
gallbladder

Such individuals excrete the organisms in their feces either continuously
or intermittently

They become an important source of infection for susceptible persons

The carrier state may be terminated by antimicrobial therapy if
gallbladder infection is not evident

Otherwise, cholecystectomy has been the solution to the chronic state of
enteric carriers

SALMONELLA
CARRIER STATE-TYPHOID MARY
 Mary Mallon (Mallone): Irish-born cook  USA
 Worked as housekeeper for various families
 “Dishes to die for”  People became sick; fatal cases
 Health authorities  carrier  When confronted  aggressive
 In isolation hospital for 3 yrs
 Public outcry  released
 5 yrs later: typhoid outbreak
 Died in isolation at age 69
Could have been
prevented:
WASHING OF
HANDS

26
Q

Salmonella Carrier State-TyphoidMary

A

Mary Mallon (Mallone): Irish-born cook

USA

Worked as housekeeper for various families

“Dishes to die for”

People became sick; fatal cases

Health authorities»carrier

When confronted»aggressive

In isolation hospital for 3 yrs

Public outcry»released

5 yrs later: typhoid outbreak

Died in isolation at age 69

Could have been prevented:WASHING OF HANDS

27
Q

Vibrio cholera:

Microscopy and Epidemiology

A

Curved Gram-negative rod
Non spore forming
Motile by means of single polar flagellum
Salt (NaCl) tolerant - halophilic
Grow in alkaline conditions - aquatic environments

0139 serogroups
Somatic antigens O1 and O139_ produce the toxin that causes cholera V. cholerae O1  3 serotypes, 2 biotypes Poor sanitation and hygienic conditions Contaminated rivers, warmer climates

28
Q

Vibrio cholera:

Classification

A

Genus
Vibrio
Vibrio choleraeSEROVAR O:1* SEROVAR O:139* NON O:1 Non-agglutinating vibrios (NAV)
Non Cholera Vibrios (NCV) OTHER SEROVARS Non-agglutinating vibrios (NAV)
Non-cholera vibrios (NCV)
Biotypes Classic El Tor Serotypes
Ogawa Inaba
Hikojima OTHER SPECIES V. parahaemolyticus
V.vulnificus
Vibrio cholerae
CLASSIFICATION

29
Q

Vibrio cholera:

Pathogenesis

A

Virulence factors:

  • Mucinase, adhesins , enterotoxin
  • Cholera toxin
  • Consist of A-B subunits
  • Binds to intestinal epithelium
  • Binds to ganglioside receptors activating adenyl cyclase
  • Overproduction of cAMP
  • Massive watery diarrhoea
30
Q

Vibrio cholera:

Clinical Manifestations

A
Incubation period: 2–3 days
Mainly through contaminated water
Improperly preserved and handled
foods, including fish and seafood,
milk, ice cream, and unpreserved
meat, have been responsible for
outbreaks
 Acute onset:  Profuse watery diarrhoea
 Tenesmus
 Abdominal pain
 Sometimes vomiting
 Neither white cells nor blood in
the stools-Non inflammatory
 Fever: < 5% of ptsRice water stools
 10–30 per day  up to 20 liter  10% of cases: rapid, severe dehydration
Electrolyte imbalance
 Metabolic acidosis, hypovolaemic shock
 Renal damage, death  Without rehydration:  Mortality rate 40–60%
 WITH REHYDRATION: < 1%
Vibrio cholerae
31
Q

Vibrio cholera:

Diagnosis

A

Clinical diagnosis in outbreaks & endemic areas

Alkaline peptone water (enrichment media
before subculturing on the TCBS)

Grow in thiosulfate citrate bile salts
sucrose (TCBS) medium to form yellow
colonies (V. cholerae)-ferments sucrose

Biochemical tests, Oxidase positive

Grow under aerobic and anaerobic
conditions

Specific antisera required for complete
identification-Polyvalent 01

32
Q

Vibrio cholera:

Treatment and Prevention

A

Rx: rehydration NB NB NB NB

Mild cases usually Oral Rehydration Therapy

Severe cases: IV

Role of antibiotics – shortens symptoms & carriage of organisms:

  • Azithromycin, ampicillin, tetracyclines, trimethoprim, and chloramphenicol
  • Most strains are susceptible to doxycycline or ciprofloxacin

Boiling and chlorination of water during epidemics are required

Adequate cooking