TM: Protozoa (i)

Intro

eukaryote (not bacteria)

biologically diverse

many mobile

unicellular

may cause disease in humans (in gut)

common worldwide

several complex biological classification systems

faecal oral tranmission

Types of diarrhoea

watery

SI

e.g. giardia

often a/w flatulance (gas + bubbles) + steathorrea (white/grey great fat)

dysentery

large intestine

blood + mucus

e.g. amoeba or shigella (bacillary dystentery)

Most famous

P falciparum - malaria

Giardia + amoebae - diarrhoea + dysentery

toxoplasma gondii - brain lesions in people with AIDS

cryptosporidia - prolonged watery diarrhoea

trypanosoma - sleeping sickness + nagana in cattle

amoebae intro

in ponds + pools

most that effect humans live in large intestine

lots of nuclei

entamoeba dispar

benign non-pathogenic versions on E histolytica

in bowel

requires no tx

endolimax nana

non-pathogenic

occurs in humans, primates, pigs

entamoeba coli

non-pathogenic (no tx)

dientaoeba fragilis

aberrant trichomonad

can cause symptoms

Entamoeba histolytica 1

strictly a human pathogen (no intermediate host/vector)

dysentry + extracolonic disease (e.g. amoebic liver abscess - liquid cystic cavity seen on CT, purulent, RUQ pain, pleuritic pain)

microscopically identical to E dispar

adult form = trophozoite

20-40microm

cytoplasm vesicles can contain RBCs

can move 5microm/s

life cycle

  1. mature cysts ingested
  1. non-invasive colonisation
  1. intestinal + extra-intestinal disease (ectopic - liver, skin, brain)
  1. cysts + trophozoites passed in faeces

hence hygiene, sanitation, pit latrines NB

worldwide distribution

a/w poor hygiene

50 million cases + 70 000 deaths / yr

10% of asymp carriers will develop invasive disease

faecal-oral route (sexual transmission also possible)

higher risk in institutions

almost any tissue can be affect - commonly liver, intestinal mucosa, brain, skin

causes goblet cells to over secrete + deplete themselves of mucin, leaving them vulnerable to infection

lysis of cells + deeper invasion occurs

ulceration of bowel mucosa

can spread in blood to other organs

90% will clear infection in 1 yr

10% develop extra-intestinal infection in 1 yr

multiple factors influence the disease to become symptomatic

intestinal features

usually insidious onset (gradually gets worse)

diarrhoea in 94-100% (often without blood initially)

abdo pain/discomfort

tenesmus (recurrent/continual inclination to evacuate bowels due to ulcerated rectum, pain inside anus upon passing stool) in 50%

"skip lesions" (patchy intestinal damage/ulceration)

rarely perforation, severe bleeding from blood vessel, inflamm polyposis

weightloss, fever, mild hepatomegaly

fulminant colitis may develop (similar to IBD i.e. UC/Crohn's - important to excl infection before dxing these)

amoeboma may develop

amoebic granuloma

inflamm, lymphocytes, macrophages

risk of bacterial superinfection

may be mistaken for mass/tumour

liver abscess

most common form of extra-intestinal amoebiasis

20% give hx of dysentary

more common in adults + males

lower SE group

thin-walled, necrotic centre with thick fluid (chocolate syrup, anchovy paste)

parasites detected in faeces 50% of time, or 75% if stool cultured

rapid onset of RUQ pain

radiates to shoulder + scap

worse when lying on right side

fever, rigors, sweats

cardinal (major) sign = painful hepatomegaly

dDx: acute surgical abdo, pyogenic liver abscess. right lower lobe pneumonia

surgical aspiration can be dangerous

leakage (infection dissemination)

transversing a blood vessel or bile duct (leaks into peritoneum)