Infections of Gastrointestinal Tract Flashcards
What is Gastroenteritis?
A syndrome characterised by GI symptoms; including
- Nausea
- Vomiting
- Diarrhoea
- Abdominal discomfort
What is Diarrhoea?
What does blood/pus in diarrhoea indicate?
Abnormal faecal discharge –> characterised by frequent and/or fluid stool
- Usually from disease in small intestines, increased fluid and electrolyte loss
Diarrhoea with blood + pus –> usually due to enterotoxin production –> indicates invasive infection with mucosal destruction
What is Dysentery? (definition)
An inflammatory disorder of the GI tract often associated with blood and pus in the faeces.
Accompanied by symptoms of;
- Pain
- Fever
- Abdominal cramps
Usually a disease of the large intestine.
What is Enterocolitis?
Inflammation of mucosa of both small & large intestine
What are the host defences in the GI tract?
- Macrophages within lamina propria
- Lymphatic vessels drain Lamina Propria into mesenteric lymph nodes. Dendritic cells enter lymph node & activate T-cells
- Active immune response –> Neutrophil recruitment
Host does the GI tract not stay in a constant state of inflammation? 5 Mechanisms (Long answer)
- GI immune system is anti-inflammatory. Commensal bacteria directly help to keep the immunosuppressive environment of the Lamina Propria
- The macrophages located within the Lamina Propria are anti-inflammatory. These do not secrete cytokines. They can deal with leaks of commensal bacteria into the LP and ‘minor attacks’ from foreign pathogens.
- IgA antibodies - specialised antibody specifically designed to protect mucosal surface & not cause inflammation. Produced by B-cells in LP.
IgA can be transported into lumen of intestine & binds to microbes to prevent them adhering to the mucosal epithelia. They can bind to microbes within the LP and transcytose them back out into the lumen - ‘escort’ - Compartmentalised response - Separate from systemic immune response. Activated dendritic cells travel to mesenteric lymph nodes - but do not travel further. Likewise, the B & T cells activated within the mesenteric lymph node only enter the Lamina Propria
- Distributed response - B & T cells are distributed throughout the Lamina Propria. The presence of lymphocytes (& IgA) allows a very fast response that can deal with infection before microbe multiplies. Limiting the number of microbes will adjust the inflammatory response.
How do the immune response become elevated?
Dendritic cells in the LP constantly sample the microbial environment.
(ALTHOUGH NOT FULLY UNDERSTOOD)
The dendritic cells can distinguish between commensal, pathogenic and low-level microbial infiltration.
If dendritic cells discover a pathogenic invasion - it will produce IL-6 which causes T-Helper cells to become Th17 cells –> which are highly inflammatory.
They also have the ability to produce cytokines that strengthen the tight junctions between epithelial cells and stimulate mucus production & facilitate the transcytosis of IgA.
Tell me about diarrhoea caused by C. difficile
Clostridium difficile is a commensal bacteria.
Antibiotic treatment disrupts normal flora - however, C. diff survives as it is spore forming. Spores germinate after antibiotics. Rapid growth. Produces two toxins (AB exotoxins)
A: alters fluid leading to water diarrhoea
B: Kills epithelia leading to pseudomembranes
Diagnosed by: Stool specimen - toxin present in faeces
Treatment: Withdraw causative antibiotic and replace with narrow spectrum.
Common in hospital patients.
What is Cholera?
Symptoms:
Rice water diarrhoea
Caused by: Vibrio cholera
Pathogenesis:
Large number of bacteria digest mucous lining of intestinal cells and then attach proximal to small intestines. Secretes AB5 endotoxin. B: binds to Gs G-protein - activating adenylate cyclase –> which converts ATP –> cAMP –> Activates pKa –> Overactivation of CFTR. Crypt cell increases Cl- secretion and villous cells absorb less Na2+ - watery diarrhoea.
Diagnosis: Symptoms, stool culture
Treatment: Rehydration & antibiotics
What is dysentery? (pathology)
Symptoms: bloody diarrhoea
Caused by: Shigella dysenteriae bacteria (-ve facultative anaerobe rod)
(Shigella has 4 known serogroups - cause shigellosis)
Pathogenesis:
Invades mucosal epithelial cells –> rarely penetrates deeper. Once inside the cell –> surrounded by membrane bound vesicle from host-cell –> vesicle is lysed by plasmid encoded hemolysin –> contents of vesicle released into cytoplasm. Can produce a neurotoxic, entertoxic and cytotoxic toxin, which inhibits protein synthesis –> host cell dies –> spreads to adjacent cells –> damage attracts leukocytes –> causes release of blood & mucus –> leading to dysentery.
Diagnosed by: Stool culture, H2S breath test
Treatment: Oral rehydration & if severe - antibiotics
What is Shigellolosis?
Conditions caused by shigella bacteria.
Particularly common & can cause problems in areas with poor hygiene where epidemics occur.
Shigella –> Grram -ve bacilli with 4 recognised serogroups:
Group A: Shigella dysenteriae
Group B: Shigella flexneri
Group C: Shigella boydii
Group D: Shigella sonnei
Shigellolosis characterised by bloody faeces associated with intestinal pain - incubation period of 1-3 days.
Main mode of transmission - person to person
What is Typhoid Fever?
Symptoms: Can be asymptomatic
- Enteric fever (spots on abdomen, fever, diarrhoea and pain)
Faecal oral transmission
Caused by: Salmonella typhi
Pathogenesis:
Large number of bacteria overcome gastric acid - bacteria enter mucosa through distal ileum or colon, Survives in peyer patches, phagocytosed –> carried to gall bladder and other organ –> releases endotoxin.
Stages of Typhoid Fever: (4)
- Slow rising temperature
- Relative bradycardia
- Malaise
- Headache
- Cough
- in 1/4th of cases - epistaxis
- Slow rising temperature
- Continuing high temperature
- Considerable weight loss
- Bradycardia continues
- Delirium is frequent
- Frequently calm –> sometimes agitated
- Continuing high temperature
- A number of complications can occur:
- Intestinal haemorrhage due to bleeding
- Intestinal perforation
- Encephalitis & high fever
- Dehydration increases delirium
- Lies motionless with eyes half open
- A number of complications can occur:
- Defervescence commences that continues into 4th week.
diagnosed by: H2S producing test
Treatment: antibiotics; remove gallbladder for carriers.
Live attenuated vaccine for travellers
I
Salmonellosis
Symptoms:
- Can be asymptomatic
- Nausea & vomiting
- Abdominal cramps
- Diarrhoea
- Fever
- Chills
- Headache
- Blood in stool
Caused by: Salmonella entericae
Pathogenesis:
Attaches to epithelium lining the small intestine –> triggers endocytosis - multiples within vesicle.
–> produces toxin to inhibit immune system –> kills host cell inducing inflammation, fever, cramps & diarrhoea
May spread to blood stream - bacteraemia
diagnosed by: stool sample
Treatment: Supportive
Does not respond well to antibiotics.
Tell me about the Salmonella bacteria
Gram -ve bacilis of enterobacteriaceae family
- -> Normally all human pathogen salmonella grouped under S. enterica
- -> further classified by their O (cell wall) and H (flagellar) antigens
Salmonella can cause two diseases:
- Typhoid fever (salmonella typhi)
- Salmonellosis (S. enterica)
What is Bacterial gastroenteritis?
Symptoms: Gastroentritis symptoms
Caused by: Campylobacter (gram -ve rods)
Campylobacter jejuni most common (due to contaminated food)
Pathogenesis:
Bacteria possess adhesins & produces an enterotoxin similar to STa produced by e.coli. As well as a number of cytotoxins
–> survives after endocytosis
–> incubates for 2-5 days and causes an enterocolitis that leads to bloody diarrhoea & fever.
Diagnosed by: Stool culture
Treatment:
Severe treated with macrolide antibiotics such as erythromycin
