6,1: gastroenteritis

gastroenteritis

inflammation of the mucus membranes of the stomach and intestines characterised by nausea, vomiting, diarrhoea, abdominal discomfort

diarrhoea

abdominal faecal discharge. more frequent and or fluid stool than normal. causes increase in fluid and electrolyte loss.

diarrhoea without blood and pus caused by

enterotoxin production

diarrhoea with blood and pus

indicates mucosal destruction by invasive infection

dysentry

inflammatory disorder of GIT causing blood and pus in faeces. pain, fever, abdominal cramps. disease in LI

enterocolitis

inflammation involving inflammation of mucosa of intestines

sample analysis

detects presents of pathogenic organisms. fresh stool collected in sterile container not contaminated with urine or water. labelled with pt name, time, date of stool collection. once allocated, sent to lab ASAP or refrigerated. stool culture test allows detection of pathogens in stool when applied to nutrient selective media.

Commensial bacteria may adhere to epithelia lining intestinal system but does not cross barrier unless there is a break then it may cross to lamina propria. what host defences are activated if this happens

1. macrophages most abundant in lamina propia which intercept the microorganisms.

2. lymphatic vessels drain the lamina propria into mesenteric lymphnodes. bacteria can be transported into lymphnodes. dendritic cells in surrounding tissues enter lymphatic vessels and travel to mesenteric lymphnodes. upon site of invasion, dendritic cells activate T cells specific for the pathogen. effector cells triggered to return back to lamina propria.

3. active immune response will cause neutrophil recruitment increasing lymphocyte entry to lamina propria.

bacteria are constantly breaking epithelial barrier why is there no chronic inflammation

GI system is anti-inflammatory as commensial bacteria maintain immunosuppressive level in lamina propria. macrophages in lamina propria are non-inflammatory as they do not secrete cytokines. IgA antibodies produced by B cells are specifically designed to protect mucosal surface and does not cause inflammation. IgA can transcytose snd can bind to microbes in LP and escort them back into intestine for disposal

compartmentalised response

dendritic cells travel to mesenteric lymphnodes but do not travel further. unique as it separate from systemic immune system. only b&t enter LP

distributed response

B&T distributed throughout LP. presence of lymphocytes and IgA therefore very fast response and deal with infection before microbe can multiply in number therefore limiting the number will adjust inflammatory response.

elevated immune response

dendritic cells in LP constantly sample microbial environment and can distinguish between commensial, pathogenic, low level of microbial inflammation. dendritic cell and pathogen then causes the release of IL-16 and Tcells release TH17. strenghthen tight junctions between epithelial cells, secrete mucus production, fascilitate transcytosis of IgA antibodies.

Traveller's diarrhea

up to 90% bacterial. acute onset. 24-72 hours after ingestion. mild cramps, urgent, loose stools, severe abdominal pain, fever, vomiting, bloody diarrhoea. protazoal pathogens take 1-2 weeks unless cyclospora cayetanensis

food poisoning

any illness from consumption of food. ingestion of toxins. organisms can be destroyed during food prep but toxins are not. nausea, vomiting, diarrhoea, cramping.

staphylococcus infections

commensial bacteria can be shed from food. salt tolerant and toxins heat stable. s.aureas can produce enterotoxins a-e stimulate contractions, nausea, vomiting. mild and self limiting. toxins resistant to destruction by stomach and SI enzymes. replacement of fluids and electrolytes. infections from ingesting pathogens can remain in GI or spread to other systems.

Food associated infections

acts as vehicle for pathogen. campylobacter can multiply to produce numbers large enough to cause salmonella disease

viral gastroenteritis

milder symptoms than bacterial gastroenteritis. calciviruses eg noroviruses

bacterial gastroenteritis

Campylobacter. G-ve. slender. spiral rods. common cause of diarrhoea especially milk, poultry, water. posess adhesins, enterotoxins, cytotoxins. can survive after being endocytosed. endocolitis with watery, bloody diarrhoea and fever. macrolide antibiotics. 4-quinolones for invasive infections.

acute gastroenteritis

profuse water diarrhoea often causing nausea and vomiting without localised findings.

definition of diarrhoea

passage of three or more loose or liquid stools per day or more frequent passage than is normal for the individual.

helminths infections of GI

nematodes: round bodies worms eg roundworms, hookworms, whipworms

cestodes: flat bodied worms that are segmented eg tapeworms

trematodes: flatbodied worms that are nonsegmented eg flukes.

ascaris lubrocoides

giant intestinal round worms. nematodes. eggs are ingested and hatch in duodenum. larvae penetrate walls of the SI and migrate through liver to heart and lungs. lodge in alveolar capillaries and penetrate alveolar walls where they ascend to oropharynx. they return to SI and develop to adult worms, mate, release eggs into stool.

enterobirus (pinworm) F-O

nematodes. ova transferred from perianal area to formites which there have a long survival time. ingested by a new host or autoinfestation. symptoms include perianal irritation, weightloss, bed wetting. mebendazol

Trichuris trichiura (whipworm) F-O

nematodes. ingested eggs enter small bowel as larvae. 1-3 months maturation. migrate to caecum and ascending colon. attach to superficial epithelium. intense infestation can cause abdominal pain, anorexia, rectal prolapse. lemon shaped eggs with clear opercula may be identified from stool.

taenia (tapeworm) F-O

flatworms cestoda. taenia saginata associated with beef whereas solium associated with pork. pigs or cattle ingest cycts from human faeces and develop into larvae and migrate to muscle and encyst. humans consume infected meat cysts which develop into larvae then adults. intestinal blockage and nutrient deficiencies.

Ancylostoma duodenale, Necator americanus (hookworms) skin

nematodes. soil transmitted. larvae penetrate the skin. travel through blood stream to lungs, alveoli, ascend to epiglottis, swallowed, mature in SI. anaemia

schistosoma species skin transmission

trematode. human host sheds eggs with faeces or urine. eggs hatch in water and release miracidia which penetrate a snail. shed as cerceriae. penetrate human skin. migrate through blood to liver. mature, mate , migrate as pair to intestinal veins (bowel or rectum). reside and lay eggs

Schistosomiasis

allergic responses to lifestyle changes. fever, eosinophilia, lymphadenopathy, diarrhoea. pathology of bladder including haemorrhage, inflammation, infiltration, polyps, nephrosis. (s. haematobium). intestinal haemorrage and inflammation (s.japon/mansoni). eggs released by females enter hepatic circulation trapped in sinusoids

food infection

presence of bacteria or other microbes infect body after consumption

enterotoxins

highly potent. S.aureus toxins synthesised throughout logrithmic phase of growth or during transition from exponential to stationary phase. resistant to heat and acidic conditions and proteolytic enzymes

enterotoxins causing nausea

transit through mucous expelling goblet cells and epithelial cells in intestinal epithelium to lamina propria. interact with mast cells to release 5-hydroxytryptamine which interacts with vagus nerve to trigger emetic response. t-cells and neutrophils may also be involved. if vomiting main source of fluid loss, hypochloraemia can occur. if diarrhoea is more prominent, metabolic acidosis is more likely. both can cause hypokalaemia

transyctosis

postulated that enterotoxin activity could facilitate transcytosis (macromolecules transported across interior of a cell). enables toxin to enter bloodstream to and circulate through the body. allows interaction with antigen presenting and T cells that lead to superantigen activity which could lead to more severe disease.

staphylococcus and food poisoning

due to ingestion of staph enterotoxin up to 6 hours. relatively mild up to a day. can be severe. not contagious. nausea, abdominal cramping, diarrhoea.

Clostridium perfringens

colonisation and proliferation of type C clostridium perfringes. initial epithelial damage or irritation caused by secreted toxins or altered luminal environment as increases acidity. clostridium can diffuse through damaged epithelial barrier into LP high susceptibility of endothelial cells to C.perfringes therefore only small amounts results in local vascular leakage increasing leakage of blood and damage to endothelium into intestinal lumen favouring clostridium growth. high proliferation capacity induced haemorrhage, accelerated clostridium growth and toxin secretion. cytotoxic to immune cells

bacillus cereus

reheated rice. spore forming bacteria. effective dose small. projectile vomiting, nausea, diarrhoea

Viral Gastrointestinal Diseases

epithelium of small intestine. watery diarrhoea. WBC and visible blood rare. rotavirus, calicivirus, astrovirus, enteric adenovirus

virus upon entry to GI tract

interact with microbiota and use commensal gut bacteria to increase infective potential. eg LPS increases thermostability of poliovirus also enhances virus engagement of cellular poliovirus receptor increasing infectivity. enterobacter species facilitate human norovirus attachment and infection.

calicivirus

norovirus. RNA. iscohedranucleocapsid. non-enveloped. SS non segmented. ingestion of infected water or food leads to local inflammation in proximal SI. within 24-48 hours. highly infectious

rotavirus

RNA virus. isosahedral nucleocapsid. DS segmented. reovirdidea. FO. incubation 1-3 days. lasts 4-8 days. vaccine preventable

Rotavirus pathogenesis

infects villus cells of proximal SI. replicates within and lyses cells. impaired absorption of carbohydrates and nutrients. vomiting followed by diarrhoea. dehydration and hospitalisation common in young children. diagnose by EIA antigen in stool. oral rehydration or IV.