$R4NAWQB

GIT
2. Enterotoxins ↓
- Enterotoxigenic E. coli (ETEC) produce plasmid A1 subunit transfers ADP ribose from NAD to
mediated enterotoxins. GTP binding protein.
- Heat labile enterotoxin (LT) ↓
- Heat stable enterotoxin (ST) Activation of Adenylyl cyclase
3. Verotoxin ↓
- Enterohemorragic E. coli (EHEC) produce Increase in cAMP
verotoxin. ↓
- It is also called shiga like toxin due to similar Hypersecretion of Cl and inhibition or Na+
-
biological, physical and antigentic properties of reabsorption.

shiga toxin. ↓
4. Antiphagocytic capsule Osmotic secretion of H2O
- KI strain of E. coli cause neonatal meningitis ↓
due to antiphagocytic capsule. Produce watery diarrhoea
Clinical features: b. Heat stable enterotoxin

• Mechanism is similar except guanylyl
1. Urinary tract infection (60-80% of UTI)
cyclase is activated which increases
2. Septic infection of wound. cGMP concentration.
3. Septicaemia, pneumonia, neonatal meningitis and ii. Enterohemorrhagic E. coli (EHEC)
abscess formation in variety of organs. - Disease: Bloody diarrhoea (but not dysentery),
4. Gastro intestinal disease. hemorrhagic colitis, hemolytic uremic
Based on gastro intestinal manifestations, syndrome, no fever
E. coli are classified as: (04) Note: Clinically, enteroinvasive E. coli resembles
shigellosis. V
i. Enterotoxigenic E. coli (ETEC)
- Diseases: Traveller's diarrhoea, infant Pathogenesis:
diarrhoea in developing countries, watery EHEC produce cytotoxin/ shiga like toxin/
diarrhoea, nausea, vomiting, cramps, low grade verotoxin
fever. (@t for T) ↓
Pathogenesis: Consists of A and B subunit
- ETEC produces two types of Enterotoxins: ↓
a. Heat labile enterotoxin (LT) B subunit binds to the host cells of large intestine
and facilitates transfer of subunit A
• Resembles cholera toxin (CT) and is
plasmid mediated enterotoxin. ↓
Subunit A disrupts protein synthesis.
Enterotoxin is composed of 2 subunits, A and B
Damage vascular endothelium → bloody
↓
diarrhoea.
A subunit is enzymatically active, whereas B
subunit helps in binding to the GM1 iii. Enteroinvasive E. coli (EIEC)
ganglioside at the brush border of epithelial Disease:
cells of the small intestine - Dysentery with scanty blood stools; fever,
↓ cramping, more prevalent in developing
After binding, A subunit dissociates to the A1 countries.
and A2 - Resembles shigellosis clinically
FAST TRACK BASIC SCIENCE MBBS -75-

Microbiology
Pathogenesis: SALMONELLA
First attach to the surface epithelium of large Past Questions:
intestine 1. Write short notes on:
↓ a. Enteric fever (3) [05 June]
Invasion and destruction of colonic epithelium b. Widal test (3) [05 June]
↓ 2. Define Gastroenteritis. Describe pathogenesis
Dysentery and laboratory diagnosis of Salmonella typhi.
(1 +4 +5 = 10) [09 July]
iv. Enteropathogenic E. coli (EPEC)
3. Describe the pathogenesis of Salmonella typhi.
Disease: Write in detail the laboratory diagnosis of Enteric
- Infant diarrhoea (Paediatric diarrhorea) (P@P) fever. (6 +4 = 10) [05 Dec]
- Vomiting, nausea, non bloody stools. 4. Describe the laboratory diagnosis of Salmonella
Pathogenesis: typhi infection. (10) [04 June]
- Plasmid mediated adherence and destruction ♦ Produces 3-main types of disease in man but
mixed forms are frequently observed.
of epithelial cells of small intestine.
1. Enteric fever:
v. Enteroaggregative E.Coli (EAEC)
- Salmonella typhi → Typhoid fever
- Disease: Infant diarrhea in developing
- S. Paratyphi A, B & C → Paratyphoid fever
countries
2. Enterocolitis:
Laboratory diagnosis: - S. typhimurium
1. Specimen collection: - S. enteritidis
V - Collection depends on the type of lesion - S. Thompson
• Faces or rectal swab in acute diahorrea - S. Newport
- S. Dublin
• mid-stream urine in UTI
3. Septicemia: S. Choleraesuis
• Pus from wound in sterile cotton swab
Note: Salmonella enteritidis can cause osteomyelitis
• C.S.F. in pyogenic meningitis. in patients with sickle cell anaemia.
2. Microscopy
Salmonella typhi & paratyphi
- Centrifuged deposit of the collected sample is
Virulence factors:
stained with Gram staining technique
1. Endotoxin: Bacterial (lipopolysaccharide (O Ag)
- On Gram staining: Gram negative bacilli. activates TLR4 on host cells.
3. Culture: Refer cultural characteristic. - TLRs play essential role in cellular response to
4. Biochemical test: Refer biochemical reaction. bacterial lipopolysaccharide.
2. Invasins: Proteins that mediate adherence to and
5. Agglutination test:
penetration of intestinal epithelial cells.
- Colonies are confirmed by agglutination tests 3. Factors involved in resistance to phagocytosis:
with group-specific polyvalent and type a. Catalase and superoxide dismutase: protect
specific antisera of E. coli. bacteria from intracellular killing by
- Important for identification of neutralizing oxygen radicals.
enteropathogenic strain of E. coli. b. Other factors neutralise defensins (that
facilitate killing of bacteria by phagolysosomes)
-76- FAST TRACK BASIC SCIENCE MBBS
GIT
4. Factors involved in resistance to acidic pH: Enteric fever (05)

- Acid tolerance response (ATR) gene. Includes: Typhoid fever and paratyphoid fever.
5. Vi (virulence) antigen: A. Typhoid fever: Caused by S. typhi
- Surface Ag of salmonella typhi - Incubation period = 7 - 14 days usually
- Has antiphagocytic property • Clinically, it may vary from a mild
6. Flagellin: undifferentiated pyrexia to rapidly fatal
- The core of bacterial flagella disease.
- Activates TLRS on host cells and increase the • Typical features are step ladder pyrexia,
local inflammatory response. with relative bradycardia and toxaemia.
Pathogenesis [ 09, SAQ 2013 KU] • Onset is usually gradual with headache,
3 6
- Infective dose (ID50) = 10 to 10 bacilli malaise, anorexia, constipation or
diarrhoea.
- Incubation period = 7-14 days
• A soft, palpable spleen is a constant finding.
Infection is acquired by ingestion of contaminated
food, milk, water • Hepatomegaly is also common.
↓ • "Rose spots" that fade on pressure appear
On reaching gut, attach themselves to microvilli of on skin during second or 3rd weeks.
ileal mucosa Complications:
↓ - Intestinal perforation
Taken up by and invade M cells - Hemorrhage
↓
- Circulatory collapse
Penetrate to lamina propria and submucosa
- Bronchitis or bronchopneumonia
↓
Organisms are engulfed by mononuclear cells in
- Psychoses, deafness or meningitis V
underlying lymphoid tissue - Cholecystitis, Arthritis, abscesses, periostitis,
↓ nephritis, thrombosis, peripheral neuritis,
Resist intracellular killing and multiply within these osteomyelitis.
cells B. Paratyphoid fever: Caused by S. paratyphi A
↓ and B
Enter mesenteric lymphnodes - Milder form of febrile illness.
↓ - Shorter duration and incubation period.
They multiply and enter blood stream - Transient diarrhoea is commonly seen.
↓ Lab diagnosis of enteric fever (04,05,09)
Transient bacteremia 1. Specimens: Blood, feces, urine, bile and serum
↓ - Samples to be collected depends on stage of
Bacilli are seeded in liver, gallbladder, spleen, illness.
bonemarrow, lymphnodes, lungs and kidneys
Stage: Examination:
↓
1st week Blood culture
Further multiplication nd
2 week Widal test (Antibody test)
↓
Massive bacteremia 3rd week Stool culture
↓ 4th week Urine culture
Onset of clinical disease [@ BASU]
Microbiology
2. Culture: d. Bile culture: To detect chronic carrier in whom

st
a. Blood culture: In 1 week organism are present in biliary tract.
• Bacteremia occurs early in disease so blood Identification:
cultures are positive in 90% cases in first - In macConkey's agar or DCA, salmonella grow
week of fever, 75% in second week, 60% in as non lactose fermenters.
3rd week and 25% after that.
- When they are further studied by Gram
• Blood is to be collected before antibiotic staining, motility preparation and biochemical
therapy is given. reactions:
• Collected by venepuncture method with all
• Gram staining: Gram negative, non sporing,
aseptic precautions.
bacilli
• 5-10 ml of blood is collected from median
• Motility preparation: Motile
cubital vein.
• Biochemical reactions:
• This blood is transferred directly into a
blood culture bile broth. → IMVIC: - + - + (citrate negative in
• Alternatively, clot culture may also be done in salmonella typhi, S. paratyphi A)
which, 5-10 ml of collected blood is allowed to → H2S +ve (Except S. paratyphi A)
clot; serum is seperated out. Clot is broken up → Urease - Ve
with sterile glass and added to blood culture
3. Serology:
medium containing streptokinase.
- Widal test
Note: Clot culture offers a higher rate of isolation
4. Demonstration of Ag:
than blood culture as, bactericidal activity of serum is
obviated in the technique. - Sensitized staphyloccal coagglutination test.
V • After incubation overnight at 37°C, sub
5. Indirect evidence:
culturing is done on MacConkey agar or - Blood for Total Leucocyte Counts (TLC) and
DCA; colourless colonies (NLF) appear. Differential Leucocyte Counts (DLC)
Note: Castaneda's method of blood culture may be - Progressive Leucopenia with relative
adopted to eliminate risk of introducing lymphocytosis.
contamination during repeated subcultures. Widal test (05)
• The method provides both liquid and solid - Agglutination test that detects antibodies
media in one bottle (Eg. brain heart produced against S. typhi, S. paratyphi A & B.
infusion medium) it is biphasic media. Principle:
b. Stool culture: In 3rd week - When patient's serum is tested with 'O' & 'H'
• Salmonella are shed in feces throughout the suspension of S. typhi and S. paratyphi, there
course and even in convalescence with occurs Ag-Ab reactions and agglutination is
varying frequency, so stool culture is also visible.
valuable.
Antigens used:
• Media: MacConkey's agar, DCA, tetrathionate.
- H & O of S. typhi
c. Urine culture: In 4th week
• Salmonella are shed infrequently in urine - H of S. paratyphi A and B
so, urine culture is less useful as compared Note: Paratyphoid O isn't used as they cross react
to blood and stool cultures media: with typhoid 'O' Ag by sharing factor XII.
MacConkey's agar.
GIT
Procedure: SHIGELLA
- Widal track with four rows of test tubes for 4 Past Questions:
Ags is used.
1. Discuss the aetiology and laboratory diagnosis in
- Serial two fold dilution of serum (1/10, 1/20, a case of bacillary dysentery. (3 + 7 = 10) [07 July]
1/40) is added to all the test tubes and equal 2. Write short notes on laboratory diagnosis of
volumes of Ag are then added to respective bacillary dysentery. (5) [09 July]
rows.
♦ Causative agent of bacillary dysentry.
- Incubated at 37°c for 4 hrs and then at 4°C
Classification (07)
overnight.
Antigenically classified as:
Observations:
1. Group A (S. dysenteriae)
- H agglutination: Loose cotton woolly clumps.
2. Group B (S. flexneri)
- O angulations: Granular disc like at bottom.
3. Group C (S. boydii)
Interpretation:
4. Group D (S. sonnei)
- No single titre is diagnositic
Morphology:
- Rising titre is important: A fourfold rise is said - Gram negative bacilli
to be diagnostic.
- Non motile, non and flagellated, non capsulated.
- In a single test, a titre of 100 of 'O' or more and
- Measures: 1-3 × 0.54m
titre of 200 of 'H' agglutinin signifies presence
- Fimbrae may be present.
of active infection, but that has to be
interpreted taking into following factors. Culture characteristic:
- Aerobes or facultative anaerobes with a growth
- Local titre, immunizations, Anamnestic
temperature range of 10-40°C and pH 7.4.
reaction, non specific Ag's, antibiotic
1. Nutrient agar:
treatment, carriers. V
• Colonies are 2mm in diameter, circular,
Note: Anamnestic reactions are due to 'H' Ags. convex, smooth and translucent.
Identification of carriers: 2. MacConkey's agar: Colorless colonies except
- Carriers can be convalescent carriers or Sh. sonnei which is a late lactose (beyond 24
healthy carriers. hours) fermenter
- They can excrete the organisms in feces, less Selective media:
commonly in urine for about 2 months to a 1. Deoxycholate citrate agar (DCA) media
year. • Same as MacConkey's agar.
i. Repeated stool culture. 2. Salmonella shigella agar
ii. Bile aspiration and culture, duodenal • Contains high concentration of bile salt →
drainage cultures. inhibit gram +ve bacteria and coliforms.
iii. Detection of Antibody to Vi Ag (1:10 or • Colourless colonies are formed.
above) in serum. Biochemical reaction:
Enteric fever: Control measures: 1. Fermentation:
a. Sanitation measures and personal Hygiene - Ferment glucose with acid production. (except
b. Immunization: flexneri)
i. Killed S. typhi vaccine: TAB vaccine - Mannitol is fermented by all except sh.
dysenteriae.
ii. Live oral typhoid vaccine: TY 21a
- Lactose is not fermented except S sonnei.
iii. Purified Vi polysaccharide vaccine.

Microbiology
2. IMViC: - + - - ↓ ↓
3. Catalase: Positive, except Sh. dysentria type I. Severe diarrhoea Bleeding from
Virulence factors: and toxaemia mucosa
1. Invasion plasmid antigen:
↓
- Mediate attachment and penetration of
Ulcer is covered by pseudomembrane formed by
mucosal epithelial cell or colon.
fibrin, leucocytes, cell debris, necrosed epithelia and
2. Toxins:
bacteria
a. Endotoxin
• Release after autolysis Clinical syndrome:
• Triggers inflammation 1. Dysentry: frequent painful passage of low volume
b. Exotoxin stools containing blood, pus and mucous with
abdominal cramps.
• Also called shiga toxin.
• Released by sh deysentraie type I. 2. Complications: Polyneuritis, myocarditis, joints-
• Toxin consists of binding (B) and active (A) effusion, hemolytic uraemic nephritis.
subunits. Laboratory diagnosis (07,09)
• It has 3 types or toxicity: Enterotoxicity, 1. Specimen collection: Fresh stool, mucous flakes,
neurotoxicity, and cytotoxicity. rectal swabs.
Pathogenesis: 2. Stool examination:
- Shigella is highly acid resistant: 10 - 100 bacilli i. Macroscopic: Odourless stool mixed with
are able to produce clinical features. blood and mucous.
Food or drink contained with shigella ii. Reactivity: Alkaline
↓
iii. Microscopic: Abundant cellular exudates,
Reach terminal ileum and colon as they resist gastric pH
bright red RBCs, epithelial cells, macrophage.
V ↓
3. Culture: Refer cultural characteristics
Attach themselves to the epithelial cells and
gradually taken by the epithelial cells where they 4. Biochemical test: Refer biochemical reactions.
multiply 5. Detection of endotoxin: Limulus test
↓ 6. Slide agglutination test: Done by using polyvalent
Colonization of the bacilli occurs laterally in adjacent antisera of three groups (A, B and C) of shigella
cells and in lamina propria and antiserum of group D (S. sonnei), one by one
↓ against the isolate.
↓ ↓
Liberate shiga toxin Autolysis of bacilli and release of
VIBRIO CHOLERA
which has 2 subunits: endotoxin Past Questions:
A&B ↓ 1. Describe the laboratory diagnosis of Vibrio
↓ Trigger acute inflammatory cholera. (5) [10 Jan]
B subunit helps in reaction 2. Describe etiology, mode of infection clinical
binding to host cells ↓ features and laboratory diagnosis of cholera.
whereas A subunit Micro-abscess formation with (1+2+2+5=10) [08 July]
disrupt protein capillary thrombosis
3. Describe the morphology and cultural
synthesis ↓
characteristics of Vibrio cholera. Write the
↓ Necrotic epithelia is soft and friable
pathogenecity and laboratory diagnosis of
Damage vascular and is sloughed out in patches
cholera. (2+2+3=10) [07 Dec]
endothelium forming Serpiginous ulcers

GIT
4. Enumerate bacterial causes of diarrhoea. - Very actively motile, single polar flagellum and the
Elaborate the mechanism involved in case of movement is of "darting type" [MCQs 2013 KU]
Vibrio cholera. (3+7=10) [06 Dec] - Is stained mucous flakes or cholera stool, the
5. Differences between classical and EI Tor Vibrios. vibrios are derranged in parallel rows; described
by Koch as "fish in stream" appearance.
[04 Dec]
Pathogensis (07)
Classification: - IP = 6 hrs-3days
VIBRIO - Faeces & vomitus of human cases or carriers
are the main sources of infection.
Group A (Cholera & Group B: Unrelated to - Infection occurs by ingestion of contaminated
cholera like vibrios) cholera vibrios, food and water.
Common H Antigen biochemically & Mechanism:
(Vibrio cholera) Antigenically - Cholera toxin has entirely main role in cholera.
(on the basis of 'O' Ag)
- Potent enterotoxin.
O subgroup I (V. O subgroups II, III, IV, - Very much similar to heat stable toxin of E. coli.
cholera 01) V & VI - It has two parts:
(Non -01 V. i. A subunit with biologic activity:
cholera)(01-0139) • A subunit has 2-fragments A1& A2.
Subtype O Antigens • A1 helps in binding of A2 and B
Biotypes • A2 helps in prolonged activation of ATP.
Ogawa AB
Inaba AC ii. B subunit that facilitates binding of A
Classical El tor Hikojima ABC subunit to intestinal cell.
Contaminated → Pathogen reaches the small
(On the basis of minor Ags)
food/water ingestion intestine by escaping acid
barrier of stomach
Ogawa Inaba Hikojima V
↓
Pathogens multiply ← In an alkaline medium, in
Difference between classical & El. tor rapidly & become the presence of nutrient &
vibrios (04) actively motile bile salts
↓
Features Classical El-tor Organism liberates
1. Haemolysis of sheep RBC - + their potent exotoxin Binding of 'B' subunit of
→
known as GM1 on cell surface
2. Haemagglutination of chick - +
enterotoxin
RBC
↓
3. V.P. reaction Usually Usually (ATP → ↑ cAMP) ← Entry of 'A' subunit into the
weak or - strong + ↓ target cell
4. Susceptibility to + - Secretion of
chloride, water,
polymyxin B
bicarbonate &
5. Sensitivity to phage V - + inhibition of
Morphology (07) reabsorption of
Na, K, Cl
- Gram negative, nonsporing, non capsulated,
↓
curved or comma shaped rod with rounded or
Rice watery
pointed ends.
diarrhoea (cholera)
- Also called 'Comma' vibrio.

Microbiology
Clinical features of cholera (08) iii. Microscopy:

- Cholera is an acute intestinal infection caused 1. Rapid diagnosis by direct fluorescent antibody
by V. cholera characterized by massive watery staining of smears from liquid stool.
diarrhoea and recurrent vomiting occurring in 2. Hanging drop preparation: shows typical
severe form resulting in rapidly progressive "Shooting star"
dehydration and death if not promptly and 3. Gram staining: Typical morphology of vibrios.
adequately treated. iv. Culture:
a. Stage of evacuation: 1. Stool sample is directly plated into one or more
V • Profuse, painless effortless, watery selective media like BSA, TCBS or Monsur's
diarrhoea, followed by vomiting. GTTA medium.
2. Specimens received on holding transport medium
• The patient may pass as much as 40 stools
are first inoculated into enrichment media such as
in a day which is Rice watery in nature
alkaline peptone water and incubated for 6-8 hrs
b. Stage of collapse (Due to dehydration) before plating on a selective media.
• Sunken eyes, hollow cheeks v. Identification: Can be done by:
• Loss of skin elasticity a. Cultural characteristic in Media (07)
• Shallow & quick respiration Media Characteristics
• Restless and intense thirst 1. MacConkey's - (Pale, non lactose fermenting)
• Cramps in leg. media Which may turn pink on
• Hypovolemic shock → death if not treated. prolonged incubation because
Lab diagnosis (06,07,08,10) of late lactose fermentation.
i. Specimens: 2. Blood agar - Hemolysis (+) in EL TOR vibrios
media Hemolysis (-) in classical
1. Watery stool and mucus flakes from stool.
3. TCBS - Colonies are large yellow due
2. Rectal swabs from contact & carriers.
(Thiosulphate to sucrose fermentation by V.
ii. Transport media:
citrate bile cholera strains (Bromothymol
1. Venkataraman - Ramakrishnan medium sucrose agar) blue as indicator)
2. Cary - Blair medium 4. Alkaline Bile - Colonies become 1-2mm
3. Bile peptone transport medium salt agar (BSA) diameter in size in 24 hrs.

GIT
b. Biochemical tests: i. Campylobacter media (37° for 3-5 days)

1. Fermentation: • Colonies appears: Circular, convex and
• Non lactose fermenter translucent and less than 2mm in
• Ferments glucose mannitol, sucrose, diameter.
maltose & mannose catalase & oxidase (+) Biochemical Reactions:
• Form indole and reduce nitrates to form - Oxidase, urease and catalase positive.
Nitrites.
- Also produce DNAase, alkaline phosphatease
2. Cholera red reaction: +ve and glutamyl amino peptidase.
3. V.P. reaction:
Virulence factors:
• El-tor → (+)
1. Urease activity:
• Classical → (-)
- Urease dissociate urea to NH3 and CO2.
4. Hemolytic reactions:
- NH3 neutralize gastric acidity facilitating initial
• El-tor → (+)
colonization of the organism.
• Classical → (-)
2. Motility
vi. String test:
3. Autoimmune response: Bacterial antigens cross
- When a drop of 0.5% sodium deoxycholate is
placed on a clean slide and colonies of V. react with antral antigens stimulating
cholerae mixed with drop on slide, they autoimmune response.
produce viscous suspension that can be drawn 4. Protease and other enzymes like mucinase and
into a string when inoculating loop is slowly lipopolysaccharidase.
raised from the slide.
Pathogenesis:
vii. Serological test:
Infection of the H. pylori as transmitted from person
- Indirect haemagglutination assay
to person
- ELISA. V
↓
HELICOBACTER PYLORI Bacilli secrete an enzyme urease which cleaves urea
Past Questions: to release NH3 and CO2
1. Laboratory diagnosis of H. pylori (4) [06, 07] ↓
2. Write short notes on: H. pylori (3) [06, 07] Ammonia neutralize the gastric pH and makes
Morphology favourable environment for H-pylori
- Gram- negative rods ↓
- Spiral or curved bacilli With the help of flagella, bacilli move to the mucosa
- After long culture, form spheroid or coccoid and is attached with epithelial cells
bodies. ↓
- Motile due to multiple monopoloar sheathed Bacilli secrete enzymes like proteases, mucinase,
flagella polysaccharidases
- Non capsulated and nonsporing. ↓
Note: Other helicobacter posse unipolar flagella These enzymes digest and degrade gastric mucosa
Cultural characteristic creating ulcer
- Strictly microaerophilic (5% O2) & capnophilic (5- ↓
10%, CO2) There is also a superficial infiltration of
- Require high humidity for growth. polymorphonuclear leucocytes causing gastritis

Microbiology
Clinical syndrome: d. Antigen detection:

- Often it causes no problems, but it can cause • Faecal antigen is detected by commercial
i. Duodenal ulcer (90%) antigen detection kit.
ii. Gastric ulcer (60%) CLOSTRIDUM DIFFICILE
iii. Increase risk of adenocarcinoma of stomach
Past Questions:
Laboratory diagnosis (06)
1. Short notes on:
- Can be done by both invasive & non invasive tests. a. Clostridium difficle. (5) [08 Jan]
1. Invasive test b. Pseudomembranous colitis (3) [07 Dec]
- Gold standard approach to the diagnosis ♦ First isolated by hall and 'O' tool from faeces of
- Involves gastric intubation, endoscopy and newborn infants.
biopsy
Habitat
i. Endoscopy
- Found in feces of 3-5% healthy adults.
• Reveals pathological change - 40-50% in feces of healthy infants.
• Character & location of ulcer can be found out. - Colonization is favored by preexisting GI
ii. Biopsy: disease and environmental contamination
• Mucosa is taken out which can be tested by: Morphology:
a. Rapid urease test: - Gram (+)ve rod
1. Biopsied tissue is placed into a small - Oval & subterminal spore
quantity of urea-containing broth to Toxins:
which pH indicator has been added.
1. Enterotoxin (toxin A) → Causes gut symptoms
2. Urease released by bacilli increases gastric
pH, which is detected by indicator. 2. Cytotoxin (toxin B) → Causes cytopathic effect
in cell cultures.
V 3. Most rapid and dependable
- Both toxins important in pathogenesis of
b. Microscopy
clostridium difficle associated disease
1. Gastric mucosa is stained by Gram stain
Pathogenesis (07)
or Giemsa stain or Warthin - starry silver
staining - It can cause:
2. Gram staining - Gram negative rods 1. Antibiotic associated diarrhoea:
c. Culture: (Refer to cultural characteristics) Use of antibiotics (Amphicillin, tetracycline,
Usually not done for diagnosis chloramphenicol, lincomycin, clindamycin)
d. Molecular tests: DNA hybridization, PCR ↓
Alter the balance of normal flora of gut
2. Non-invasive tests:
↓
a. Serology:
It favors colonization and multiplication of C. difficile
ELISA: detection of antibody
↓
b. Urea containing an isotope or carbon (Carbon14) Production of toxin in colon of carriers
is fed to the patient → Urease break it into C14O2
↓
and NH3→ expired C14O2 is detected.
i. Diarrhoea (Watery & profuse, sometimes
c. Urine test: bloody)
• Radioactive isotope of nitrogen (N15) is ii. Colicky abdominal pain
incorporated to urea. Urea after broken iii. Body temperature is > 39°C
yields N15H3 which dissolves in H2O to form
N15H4OH. This is passed in urine which can Note: In most cases, the imbalance of normal flora
be detected by mass spectrometry. subside after therapy.

GIT
2. Pseudo membranous colitis: VIRAL DIARRHOEA

Enterotoxin
Past Questions:
↓
Accumulation of inflammatory exudates 1. Diarrhoea associated viruses. (3) [07 July]
composed of polymorphonuclear leukocytes, 2. Discuss pathogensis and laboratory diagnosis of
fibrin & mucin is attached to mucosal surface
Rota virus. (2+3=5) [11July,10 July]
↓
Gives membrane like appearance when viewed via 3. Write short notes on morphology of Rota virus.
colonoscopy (3) [07 Dec]
Note: Lincomycin and clindainycin are most
♦ Virus responsible (07)
important offending agents of colitis
- Rota virus
Lab-diagnosis:
1. Colonoscopy: Pseudo membrane can be seen - Norwalk virus
2. Direct demonstration of toxin in feces and - Adenovirus
patient: By inoculation of cell cultures of
- Calcivirus
difficile toxin
3. Isolation of organism: From feces by - Astrovirus
inoculating in selective media with subsequent - Sapovirus
test for toxigenecity
Primary age (great Clinical
Virus Family Genome Size Symmetry Envelope
risk) severity
1. Rota virus Reoviridae dsDNA Children < 5yrs +++ 70nm Icosahedral Absent
segmented
V
2. Norwalk virus Calciviridae ssRNA All ages ++ 27 nm Icosahedral Absent
3. Sapoviurs Calciviridae + ssRNA Children <5 yrs + 30 nm Icosaheadra Absent
4. Adenovirus Adenoviridae dsDNA Children <5 yrs + 80 nm Icosamedral Absent
(Type 40 & 41)
5. Astrovirus Astroviridae +ve ssRNA Children < 5yrs + 38 nm Icosahedral Absent
6. Calcivirus Calciviridae ssRNA Children + 35 nm Icosahcdral Naked
Rota virus - Rota virus group is most common, causes 90%
of infection.
Morphology (07)
- Member of Reoviridae family
Pathogenesis (10,11)
Mode of transmission:
- Non enveloped, dsRNA virus with icosahedral
symmetry. - By fecal oral route
- RNA consist of 11 segment - Season: winter
- Electron microscopy shows two type of rota - Age Group:
viruses, complete and incomplete particles. • <5 yr of age
- The virus has the characteristic wheel like Note: By age of 6 yr, majority of children have
appearance. antibodies to at least one serotype.

Microbiology
- Incubation period: 2 - 4 days ♦ Only the virus with a fibre protruding from each of
Ingestion of Rota virus the 12 vertices of the capsid.
↓ ♦ The fibre is the organ of attachment and is a

Bind to lactose receptor in brush border in small haemagglutinin.
intestine ♦ There are 41 known antigenic serotypes.
↓ ♦ The fibre protein is main type specific antigen.
Infection of mature enterocyte ♦ Type 40 and 41 cause infantile gastroenteritis.
↓ Laboratory diagnosis:
Cell death and villous atrophy I. Adenovirus antigen detection in patients stool.
↓ II. Isolation of the virus in cell culture
↓ ↓
III. Detection 4-fold or greater rise in Ab titre
Reduced digestion and Crypt hyperplasia
Astrovirus
absorption of nutrient ↓
♦ Linear, positive sense ssRNA virus
↓ Hypersecretion of water
Primary malabsorption into lumen ♦ The surface of the icosahedral capsid has five or
six pointed star appearance.
↓ ↓
♦ Causes outbreak of diarrhoea in children under 5 yr.
Non absorptive diarrhea Watery diarrhea
♦ Mild gastroenteritis.
Note: No inflammation occur and the diarrhoea is ♦ Transmission: By fecal oral

non bloody ♦ Diagnosis: Detection of viral antigen.
V Norwalk virus
Clinical feature:
- Nausea, vomiting and watery, non bloody ♦ Membrane of calciviridae
diarrhoea ♦ Genome: Positive sensed SSRNA
- Dehydration: main complication ♦ Viral size: 27 nm
Laboratory diagnosis (10,11) Pathogenicity

I. Specimen - Mode of transmission: By fecal oral route.
a. Stool collected in dry container, emulsified in - Incubation period: 24 - 48 hrs

buffered saline - It is cause of epidemic viral gastroenteritis in
adults, rapid onset diarrhoea, vomiting, nausea
b. Rectal swab (for unconscious patient)
etc.
II. Electron microscopy: demonstrates virus
Laboratory diagnosis:
III. Viral antigen: By CFT, ELISA
- Demonstration of virus: Electron microscopy
IV. Antibody titre: Is measured by ELISA
- Viral antigen detection: by ELISA
V. Viral genome detection: RT - PCR
- Antibody detection by ELISA
Adenovirus • 4 fold rise of Ab-titre in paired sera
♦ Non enveloped DNA virus with icosahedral capsid indicates recent infection.

GIT
PARASITES (GIT PARASITOLOGY) - Parabasal bodies: Two curved median bodies

posterior to sucking disc.
PROTOZOA (GIT) - Division: Longitudinal, following duplication of
Past Questions: all cell organelles.
1. Describe the life cycle, pathogenesis and
laboratory diagnosis of Amoebiasis caused by
Entamoeba histolytica. (3+3+4=10) [10 July]
2. Describe etiology, mode of infection, clinical
features and laboratory diagnosis of amoebic
dysentery. (1+2+2+5=10) [08 Jan]
3. Write short notes on:
a. Entamoeba histolytica. (3) [05 Dec, 04 June]
b. Intestinal protozoal parasites. (3)[08 July]
Giardia lambia
♦ Habitat: Duodenum and upper part of jejunum of
man.
♦ Morphology: Exists in two phases:
II. Cyst:
I. Trophozoite - Shape: Oval, football shaped
II. Cyst - Size: 12 × 7 µ
I. Trophozoite/vegetative form - Nucleus: 4 nuclei in cluster or lie in pairs at
opposite pole. V
- Shape: Tennis or badminton racket, or heart
shaped - Cyst wall: Tough, hyaline.
- Size: 14 × 7 µ
- Motility: Actively motile with the help of 4
pairs of flagella.
- Nucleus: Two nuclei, one on each side, nucleus
has large central endosome with no chromatin
granules on the nuclear membrane.
- Axostyle: Slender rod like structure, two in
number formed by the fusion of axonemes of
flagella and associated group of microtubules.
- Symmetry: Bilaterally symmetrical
- Dorsal surface: Convex
- Ventral surface: Concave
- Anterior end: Broad, posterior end: pointed
- Sucking disk: Present on ventrally concave
surface.

Microbiology
Life cycle: • Indefinite abdominal pain, nausea, vomiting

- Definitive host: Human beings • Steatorrhoea: Passage of yellowish and
- Intermediate host: Not required, passes life greasy stool with excess fat
cycle in one host • Malabsorption
Mature cyst - passed in feces of contaminated food • Severe flatulence
and drinks • Children: Develop chronic diarrhoea,
↓ malabsorption, wt. loss
Infection occur by ingestion of contaminated food or • Cholecystitis and jaundice occasionally
drink Laboratory diagnosis:
↓ I. Specimen:
Cyst hatches out in 2 trophozoites within 30 minutes. - Faeces should be collected in clean, wide,
↓ mouthed container and transported immediately
Multiply in intestine by longitudinal binary fission within 30 min to laboratory for examination.
↓ II. Microscopy:
When condition in duodenum become unfavourable - Saline preparation: Demonstration of motile
for survival of trophozoite form; trophozoite
↓ - Iodine preparation
Encystment occur in large intestine • To demonstrate trophozoite in killed state
↓ • Cyst in stained state
Mature cyst are passed in faeces to repeat the cycle • Only cyst are seen in asymptomatic carriers.
Pathogenicity: - Demonstration of cyst in concentrated stool
V - Mode of transmission: Fecal-oral route sample when cysts are less in number
- G. Lambia is not tissue invader. - Demonstration of trophozoites in bile
Pathogenesis aspirated duodenum (bile A) or removed from
bile duct (bile B).
Trophozoite - Colonize in the duodenum and attach
to epithelial cells with the help of sucking disk III. Serology:
↓ a. Ag-detection: By ELISA, fluorescent method

using monoclonal antibodies.
Because of tight association with epithelial cells of
duodenum b. Ab-detection: ELISA and indirect
immunofluorescence tests.
↓
Causes disturbance of intestinal function and Balantidium coli
abnormalities in villus ♦ It occur in following form
↓ I. Trophozoite/vegetative form
This leads to mechanical interference to absorption - Shape: Oval
of fat, fat soluble vitamin & haematinic factors. - Size: 60 - 70 µ × 40 - 50 µ
Clinical feature: - Motility: Motile with the help of cilia covered
- Disease caused by it: Giardiasis all over the body.
- Giardiasis → Is characterized by - Nucleus: Two nuclei, one large kidney shaped
• Diarrhoea → 5-6 stools per day - explosive (Macronucleus), one small round (micro
watery stool. nucleus)

GIT
- Anterior end: Narrow, show cytosome (mouth) ii. Intermediate host: Not required, passes life
& cytopharynx. cycle in one host.
- Posterior end: Broad, show small pore iii. Transmission: Pig to pig, pig to man, man to
(Cytopyge - anus) man, and man to pig
- Two contractile vacuoles: One in middle and Infection occurs by ingestion of cyst
other at posterior end ↓
- Many food vacuoles, tissue debris, white blood Cyst hatches out in trophozoite in large intestine
cells and red blood cells are present in ↓
cytoplasm. Multiply in intestine by binary fission and form large
II. Cyst number of trophozoites
- Shape: Oval ↓
After a period of growth and multiplication, when
- Size: Smaller than trophozoite → 50-60µ in
conditions become unfavourable for survival of
diameter
trophozoite form, encystment occur
- Nucleus: Two nuclei → Macronucleus and ↓
micronucleus
Mature cyst are passed in faeces & repeat cycle
- Cyst wall: Thick, transparent, double layered
wall.
Pathogenecity
- B. coli feeds mainly on starch, but also ingest
bacteria, RBC & epithelial cells.
- Clinical disease occurs when trophozoite
invade intestine mucosa.
- The factors that play role in pathogenesis are
i. Malnourishment V
ii. Concurrent infection
Clinical feature:
- Disease caused by it is called Balantidiasis→
characterized by
• Mucosal ulcer and submucosal abscess
- Diarrhea or dysentery with abdominal pain,
tenesmus, nausea and vomiting
- Occasionally, intestinal perforation with peritonitis
and involvement of genital and urinary tract.
Laboratory diagnosis:
i. Specimen: Stool collection
ii. Microscopy
- Demonstration of parasite in stool sample
by saline and iodine preparation
iii. When stool examination is negative, scraping
or biopsy specimen obtained by sigmoidoscopy
Life cycle: is useful in suspected cases.
i. Definitive host: Pig is the natural host, man is iv. Culture: B. Coli can also be cultivated in vitro
accidental host. like E. histolytica
Microbiology
Entamoeba histolytica (04,05) - Contain small dot like structure, central in

position called karyosome, which is surrounded
Habitat:
by clear halo.
- Trophozoite of E. histolytica inhabit in the - Nucleus is surrounded by a nuclear membrane
mucous and submucous layers of the large lined with a single layer of uniformly
intestine of man. distributed chromatin granules.
Morphology: II. Pre cystic stage
- It occur in 3 stages - It is a transitory stage, formed during the
I. Trophozoite form conversion of trophozoite to cyst.
II. Pre cystic - Shape: Round or oval with blunt pseudopodium.
III. Cystic - Size: 10-20µ
I. Trophozoite/vegetative form - Endoplasm: Free of red blood cells and other
- Is feeding stage of E. histolytica ingested particles.
- Shape: Irregular, constantly changing → No - Nucleus: Retains the features of trophozoite
fixed shaped stage.
- Size: 10-40µ (Avg. 20-30µ) III. Cyst state
- Motility: Actively motile with the help of - Shape: Spherical
pseudopodium - Size: 10-15µ
- Cytoplasm: Differentiated into Nucleus:
a. Ectoplasm: Thin, clear, translucent outer layer - Each cyst contains a single nucleus and a mass
b. Endoplasm: Granular inner layer containing of glycogen and 1-4 cigar shaped or oblong
nucleus, food vacuoles, RBCs, occasionally retractile rods is called chromatoid bodies.
WBCs and tissue debris. - As it matures, the glycogen mass and
Nucleus chromatoid bodies disappear.
- Spherical - The nucleus undergoes two successive mitotic
V - Size 4-6µ division to form 2 and finally 4 nuclei (mature
cyst-quadrinucleate)

GIT
Life cycle (10) Pathogenesis of amoebiasis (10)

- Definitive host: Human beings Ingestion food and water contaminated with
- Intermediate host: Not required, passes life quadrinucleated cyst
cycle in one host - the man ↓
Mature cyst passes in faeces of convalescents and The cyst wall resistant to Gastric juice so, the cyst
carrier contaminate food & drink wall is damaged in caecum or lower ileum by action
↓ trypsin causing excystation
Infection occur by ingestion of contaminated food or ↓
drink Releases tetranucleate amoebae followed by
↓ metacystic trophozoites
Cyst passes through the stomach undamaged and ↓
enter the small intestine Metacystic trophozoites invade the mucous
↓ membrane of large intestine due to proteolytic
Excystation occurs in the caecum or lower part of the ferment and active motility
ileum. During this period, the cytoplasm gets ↓
detached from the cyst wall, then causing a tear in Proteolytic ferments secreted
the cyst wall a tetranucleate amoeba (metacyst)
comes out Cysteine Lectin Histolysin Amoebapore
↓ Digest ECM Binds to Causes Form pore in
Nuclei and cytoplasm of metacyst divide to form 8 and degrade carbohydrat necrosis & plasma
amoebulae, which lodge in the submucous tissue of Fibronectin, e on surface destruction membrane
the large intestine where they grow and multiply by Laminin, of colonic of tissue
binary fission type I epithelial V
collagen cells
↓
Produce characteristic lesions of amoebiasis (flask
shaped ulcer) Damage mucosal epithelium and reach submucous
↓ coat, where they multiply and ↑in number and form
colonies
When condition becomes unsuitable for survival in
↓
trophozoite form, some of them get converted into Destroy the tissue in their vicinity and utilize
precystic stage and finally into cystic state cytolysed material as their food. Thus spread rapidly
↓ in various direction and dissolve surrounding tissue
and bring about coagulative necrosis by histolysin
Cysts are passed in faeces to repeat the cycle
↓
Pathogenecity Form abscess, which breaks down to form a
- Trophozoites in lumen do not cause any illness, characteristic flask shaped ulcer with a narrow neck
until they invade the intestinal tissue. and broad base
- This happens in 10% cases, 90% cases are Clinical feature (08)
asymptomatic. Disease produce is called Amoebiasis
Mode of transmission (08) a. Intestinal amoebiasis: Also called primary
amoebiasis
- Faeco-oral route
b. Extra-intestinal amoebiasis: Also called
- Infective stage: Quadrinucleated cyst
secondary or metastatic amoebiasis

Microbiology
a. Intestinal amoebiasis: 2. Diagnosis in Asymptomatic carrier (Cyst passer)

It is characterized by - Important in epidemiological surveys
- The passage of blood and mucous in stool - Demonstration of E. histoytica
• Repeated stool examination for
- Stool - foul smelling and brownish black in color
trophozoites and cysts.
- The patient is usually acerbate and nontoxic
• Concentration method: to demonstrate cysts.
- Sometime only diarrhoea and vague abdominal - Culture: Microscopically, negative stool may
symptom. give positive result by culture.
b. Extra - intestinal amoebiasis - Serology: May be positive in invasive amoebiasis.
- Hepatic amoebiasis: Difference between Amoebic and Bacillary
• Occurs in tropics in 2-10% cases of intestinal dysentery (03)
amoebiasis S.
Feature Amoebic dysentery Bacillary dysentery
• The pain and tenderness in rt. hypochondrium N.
Clinical
• Wt. loss, fever with chills
1. Onset - Gradual - Acute
- Pulmonary amoebiasis 2. Fever, - No - Fever & usually
- Cutaneous amoebiasis vomiting vomiting
- Cerebral amoebiasis 3. Frequency - 6 to 8 time per - Over 10 times/
day day
- Splenic abscess
Macroscopic
- Amoebic vaginitis
1. Odour - Offensive - Odourless
Laboratory diagnosis (08, 10) 2. Nature - Blood & mucus - Often water &
1. Intestinal amoebiasis (symptomatic pattern) bloody
I. Specimen Collection 3. Reaction - Acidic - Basic
V - Stool are collected & transported immediately
4. Color - Dark red -
(altered blood)
Bright red (fresh
blood)
II. Examination: 5. Amount - Relatively - Small
1. Stool copious
a. Naked eye 6. Consistency - Do not adhere - Adhere to
to the container bottom of
Colour: Dark brown container
Odour: Offensive Microscopic
Bloody mucus: Present 1. RBC - In clump - Discrete or in
rouleaux
Consistency: Semi fluid
2. Pus cells - Scanty - Numerous
b. Microscopy
3. Macrophages - Nil or very few - Numerous &
• Saline preparation: To demonstrate large
motile trophozoites 4. Ghost cells - Nil - Numerous
• Iodine preparation: To demonstrate 5. Eosinophils - Present - Scarce
killed trophozoites and stained cyst 6. Pyknotic - Very common - Nil
bodies
• RBC: Rouleax formation
7. Trophozoite - Present of E. - Nil
2. Blood: histolytica
Moderate leucocytosis 8. Charcot- - Present - Nil
III. Serology: Leyden
Causative E. histolytica Bacteria (Shigella)
- Negative in early cases and in the absence
agent
of deep invasion.

GIT
Complication of E. Histolytica infection - Anterior end: Thin, has mouth surrounded by 3

I. Pulmonary complication finely toothed lip.
- Empyema - Freshly passed worms: Light brown or pink in
- Pneumonia color that changes gradually to white.
- Hepatobronchial fistula - Body cavity: Present and contains ascarase or
ascaron, a toxic fluid
II. Hepatobiliary complication
Male worm:
- Hemobilia & Jaundice
- Length: 15-25cm and 2-4mm in diameter
III. Septic shock
- Has curved posterior end (tail) and two
IV. Peritonitis, ascitis
copulatory spicules
V. Cerebral amoebiais
- Life span: About 6 months.
VI. Skin: Granulomatous ulceration
Female worm:
VII. Splenic: Abscess
- 25-40cm in length and 5mm in diameter,
VIII. Amoebic Pericarditis
stouter than male with straight and conical
posterior end
WORMS (HELIMINTHOLOGY)
- The vulva is situated at the junction of anterior
Past Questions:
and middle third of the body which is narrow
1. Life cycle, pathogenesis and laboratory diagnosis and is called vulvar waist.
of ascaris lumbricoides. (3+3+4=10) [05] - It is oviparous -mature female can liberate
2. Describe the life cycle pathogenesis and about 2,00,000 egg daily.
laboratory diagnosis of hook worm. - Life span about 1yr.
(4+3+3=10) [10 Jan] - Unfertilized female is also capable of laying
3. Distinguish nematodes from cestodes. eggs. V
(5) [11 July] Eggs: Two types
4. Describe the life cycle and laboratory diagnosis of I. Fertilized egg
hook worm. (7+ 3=10) [05 June] - Shape: Round or oval
5. Write short notes on:
- Size: 60 - 70 µ× 40 - 50 µ
a. Taenia solium (5) [05 Dec]
- Colour: Yellowish - brown - bile stained
b. Morphological differences between taenia
- Egg shell: Thick smooth, translucent with an
solium and taenia saginata (5) [06 June]
uneven outer albuminous coat
c. Bile stained ova. (5) [06 June] (rugosities/corticated) this albuminous coat
d. Ascaris lumbricoides (5) [08 July] is sometimes absent (decorticated egg
e. Complication of Ascariasis (5) [04 Dec] ie.egg without an outer coat)
f. Hook worm (5) [07 July] - Ovum: Large, unsegmented ovum
g. Laboratory diagnosis of Enterobiasis (5) [04 Dec] - There is clear, crescentric area between the
Ascaris lumbricoides (08) ovum and the egg shell at each pole.
- It floats in saturated solution of common
Morphology:
salt.
Adult worm
- Covering - 3 (i) outer mamillated layer (ii)
- Shape: cylindrical with tapering ends.
middle transparent (iii) Inner lipoidal
- Size: Upto 40cm in length it is the largest
vitelline.
intestinal nematode.
Microbiology
II. Unfertilized eggs: Pathogencity (10)

- Shape: Narrower, longer and more elliptical - The disease caused by it called ascariasis
than fertilized egg.
- Most of infection (85%) are asymptomatic,
- Size: 80 - 90 µ × 45-55µ
however mild infection is clinically manifested
- Color: Brownish - Bile stained.
by intestinal disorder, malnutrition etc.
- Egg-shell: Thinner, with irregular outer
albuminous coat. - Symptom is caused by both migrating larvae
- Ovum: Small, highly refractile granules of and adult worms.
various sizes. A. Symptoms due to larvae
- It does not float in saturated solution of I. Ascaris pneumonia (Loeffler's syndrome)
common salt
• It occurs in heavy infection, which is
Life cycle (10)
characterized by fever, non-productive
- Definitive host: Human beings
cough and dyspnoea.
- Intermediate host: Not required
• The pulmonary infiltration with eosinophilia
Fertilized eggs with unsegmented ovum passed in
(eosinophils count > 20/cumm is called
faeces develop in soil, unsegmented ovum develops
Loeffler's syndrome)
into rhabditiform larva (ripe egg)
st
↓(1 moulting in soil) II. Hypersensitive reaction
Infection occurs by ingestion of food, drink or raw • Urticaria, asthma
vegetables contaminated with eggs containing
B. Symptoms due to adult worms
rhabditifom larva.
↓ - Incubation period is 60-75 days.
V Eggs are subjected to the action of digestive juice in - Infection may be asymptomatic.
the duodenum and the motile rhabditiform larvae are
- The adult worms produce pathogenic effect in
released in the upper part of the small intestine.
following ways.
↓
Rhabdiform larvae penetrate the intestinal mucosa,enter i. Nausea & vomiting
the portal circulation and reach the liver. ii. Spoliative action: Absorbs nutrition by
↓ robbing the host causing malnutrition.
After a period of 3 or 4 days in liver, the larvae enter iii. Toxication: Body fluid of Ascaris when
the systemic circulation and reach the lung via right absorbed in blood causes toxic effect and
heart.
gives rise to typhoid like fever and
↓(II & III moulting in lungs)
nd rd
hypersensitivity reaction such as fever,

From alveoli they ascend the bronchi and trachea urticaria, edema of face.
larynx and pharynx and are swallowed with saliva
iv. Mechanical effect:
↓
Finally, they reach the upper part of small intestine • Causes obstruction and perforation of
th
(IV moulting) where they grow into adult worm in 6-10 intestine
weeks and after mating, the females lay fertilized • Occasionally, obstruction of bile duct
eggs which pass out in faeces and pancreatic duct.
↓ v. Ectopic ascariasis: Can cause liver abscess
The cycle is repeated and appendicitis.
GIT
Laboratory diagnosis (08, 10) Male worm:

A. Direct evidences - Size: Smaller, 8-11 yr and 0.45mm
I. Demonstration of adult worm - Posterior end: Its posterior end has umbrella
like copulatory bursa with two copulatory
a. Adult worm can be seen when adult worm
spicules.
is spontaneously passed in stool.
- The bursa has 3 lobes: 1 dorsal and 2 lateral.
b. Administration of an anti-helminthic may
result in expulsion of worm and defecation. - These lobes are supported by 13 chitinous rays:
dorsal lobe with 3 and lateral lobes with 5 each.
II. Detection of egg
Female worm:
a. Direct wet mount: By direct saline preparation
- Size: Larger, 10-13 × 0.6mm
b. Concentration technique: Is applicable
- Posterior end: Its posterior end is tapering and
when parasitic infestation is light.
no expanded bursa is present like male worm.
c. Duodenal aspirate: Show egg
- The vulva opens ventrally at the Junction of
III. Demonstration of larva in sputum: posterior and middle third of body. It is oviparous
Can be observed in Loeffler's syndrome along with mature female can lay 10,000 - 25,000 eggs.
eosinophils and Charcot Leyden crystals Egg: (13)
B. Indirect evidences - Shape: oval or elliptical
i. Blood examination: ↑ed eosinophils count in - Size: 60µ × 40µ
early phase of infection. - Colour: Colorless, non bile stained
ii. Skin test - Egg shell: Transparent hyaline
- Content: Segmented ovum generally with 4 V
ii. Serological test
blastomeres
• Used for Ascaris pneumonia
- Floats in saturated solution of common salt
• ELISA, IHA & micro precipitation
Ancylostoma duodenale (Hook worm) (07)
Morphology
Adult worm:
Egg shell
- Shape: Small, grayish white and cylindrical
- Anterior end: Bent dorsally, hence the name
hookworm.
Blastomere
- Freshly passed worm: Is reddish brown
because of ingested blood in its intestine
- Mouth: Has 6 teeth, 4 hook like on the ventral
surface and 2 knob-like on dorsal surface.
Esophageal gland secretes an anticoagulant
ferment.
- Life span: 6-8 yr
Life cycle (10)
i. Definitive host: Human beings
Microbiology
ii. Intermediate host: Not required. B. Symptoms due to adult worms

rd
Infective stage: Filariform larva (3 state) i. Gastrointestinal symptoms:
Egg with segmented ova containing 4 blastomeres • In early phase of infection
which are passed in stool • Includes: abdominal pain, body diarrhea.
↓ ii. Chronic infection: Iron deficiency anemia,
They develop in soil to form 1st stage rhabditiform
pallor, nutritional defects.
larva
↓ 1 moulting
st
Causes of anemia
2nd stage Rhabditiform larva
Sucking of Secretion of ↑ed worm burden
↓ 2 moulting
nd
blood by anticoagulation ↓
Filariform larva (infective form)
worm at containing Deplete iron store
↓ multiple site secretary and folic acid
Infection occurs by penetration of filariform larva in gut mucusa material ↓
via the skin. Filariform larva on reaching causing ↓ Interference with
subcutaneous tissue, enter into lymphatics of bleeding Leads to iron absorption
small venules continuous from intestinal villi
↓ Via right heart bleeding from
Enter venous circulation punctured site
↓
Reach pulmonary capillaries and enter the Anemia
alveolar spaces
↓ Note:
Migrate to bronchi, trachea, larynx and pharynx - A single adult of worm of A. duodenal sucks 0.2ml
epiglottis and are swallowed in oesophagus
of blood/day
V (IIIrd moulting)
- N. americanus sucks 0.03 ml blood/day
↓
Finally they reach small intestine where they grow Laboratory diagnosis (10)
into adult worms, after IVth moulting in 3 or 4 1. Direct evidence
weeks, They sexually mature and after mating,
Examination of stool
the females lay eggs and pass in faeces
↓ a. Macroscopic examination
The cycle is repeated • Adult worm demonstration
Pathogenecity (10) b. Microscopic examination
- Disease: Ancylostomiasis (hookworm disease) • To demonstrate characteristic hookworm
- The symptoms are produced by both larvae egg.
and adult worms. • Concentration method: For light infestation
- Portal of entry: Skin penetration • <5ggs/mg of faeces → indicates light
A. Symptoms due to larvae infection.
i. Ground itch or dermatitis • >20egg/mg of faeces → indicates heavy
• Characterized by pruritic maculopapular infection.
dermatitis c. Study of duodenal contents material obtained
ii. Creeping eruption by duodenal intubation (Ryle's tube) may
• Characterized by reddish itch papule along sometimes reveal either egg or adult worm.
the path. 2. Indirect evidences
iii. Bronchitis or bronchopneumonia a. Blood examination: Shows eosinophila, anemia
GIT
b. General examination of stool: Necator Americanus

• Occult blood loss → indicates positive ♦ N. americanus is similar to A. duodenal in many aspects
• Charcot-Leyden crystals → often present with some morphological differences as follow.
Features (Adult worm) A. duodenale N. americanus
1. Size - Adult worm large and thicker - Adult worms smaller and more
slender
2. Anterior end - Bend in the same direction - Bend in opposite direction to the
body curvature
3. Buccal capsule - 6 teeth - 4 hook like teeth on ventral surface - 4 chitinous plates - 2 on ventral
& 2 knob - like teeth on dorsal surface. surface and 2 on dorsal surface
4. Copulatory Bursa - Dorsal ray is single fold number of rays - 13 - Dorsal ray is split from base. Total
two spicules, separate no. of rays - 14. Two spicules,
fused at the tip.
5. Posterior end of female - A spine is present - No spine
6. Vulval opening - Behind the middle of body - In front of middle of body.
7. Shape of buccal capsule - Elongated, pear - shaped - Almost spherical
rd
8. 3 stage larva - Longer - Shorter
9. Pulmonary reaction - More common - Less common
10. Peripheral eosinophilia - More pronounced - Less pronounced
♦ Life cycle, morphology, pathogencity and diagnosis - The posterior end is pointed
of N. americanus are similar to A. duodenale. - It is ovo-viviparous V
♦ But N. americanus is comparatively less pathogenic Eggs:
than A. duodenale. - Shape: oval
Strongyloides stercoralis - Size: 55µ × 30µ
♦ Smallest pathogenic nematode - Egg shell: Thin and transparent
♦ Habitat: Upper part of small intestine - Contain a larva ready to hatch
Morphology - Egg: Laid in the tissue and immediately
Adult worm: rhabditiform larva hatches out, and makes its
- Only female worms are demonstrated in way from the mucous membrane into the
human as male worms are unable to lumen from where it is passed in faeces.
penetrate intestinal wall and hence remain in Larvae:
the lumen of the bowel.
- These are of following two types
- Male are eliminated from the bowel by the
1. Rhabditiform larvae
time females start laying eggs.
Male worms: • Size: 200µ - 250µ in length and 16µ in
- Shorter and broader than females breadth
Female worms: • Motility: Actively motile
- 2.5mm long and 0.04 - 0.05mm brand • Mouth: Small mouth and a double bulb
- It has a small buccal cavity surrounded by 4 lips oesophagus
and 2 uteri with 5-10 eggs in each.
Microbiology
2. Filariform larvae: Infective stage Clinical manifestation

• Size: Larger and more slender than 1. Cutaneous lesions
rhabditiform larvae • Uritcarial rash
• Mouth: Short mouth, cylindrical • Erythematous urticarial wheal reaction
esophagus around the anus
Life cycle: • Larva currens
- Definitive host: Human beings. 2. Pulmonary lesions
- Intermediate host: Not required • Hemorrhages in the lungs by migrating
- Infecting stage: Filariform larvae larvae
- Portal of entry: Skin penetration • Bronchopneumonia
3. Intestinal lesion:
Entry occurs by penetration of filariform larvae in
contaminated soil through skin or mucous membrane • Intractable bloody diarrhoea with mucus
and mild epigastria pain
↓
4. Eosinophilia and moderate leucocytosis
Filariform larva reach the lungs through the blood
stream via heart and break into alveoli In Immuno-Compromised host → cause
I. Hyper infection syndrome: Represents an
↓
acceleration of normal life cycle of S.
From alveoli, they migrate to the bronchi trachea,
stercoralis leading to excessive worm burden
larynx and epiglottis, and are swallowed
without spread of larvae outside the usual
↓ migration pattern (GI tract, lungs)
Finally they reach the small intestine where they II. Disseminated strongyloidiasis: Involve wide
grow into adult worms spread of dissemination of larvae to CNS,
V
↓ heart, urinary tract which are outside the
The female lays eggs either by parthenogenesis realm of the parasite's ordinary life cycle.
(laying eggs without fertilization) or after fertilization Auto infection:
with male - It occurs when non infective rhabdiform larvae
↓ prematurely transform into infective filariform
larvae.
Egg hatch out immediately to form rhabditiform
I. Endoauto infection
larvae in intestinal mucosa and migrate into the
lumen of intestine • The larvae penetrate the mucosa of the
colon and the upper small intestine and
↓
causes endoauto infection.
The rhabtidiform larvae either pass with the faeces to II. Exo-auto infection: The larvae penetrate
soil where they develop into infective filariform the perianal skin and cause exoauto
larvae or develop into filariform larvae in the lumen infection.
and cause autoinfection (hyperinfection) in same Laboratory diagnosis:
host by penetrating mucosa or perianal skin
1. Direct evidence
Pathogenecity: a. Direct wet mount of stool: Reveals
- Disease: Strongyloidiasis rhabditiform larvae
- Most cases are asymptomatic or mild • Presence of egg: Strong evidence of
cutaneous or abdominal symptoms infection.

GIT
b. Concentration method: In case flight infection Egg:

by formol - ether method - Shape: Spherical and brown colour (bile
c. Duodenal aspiration: stained)
• Larvae can be detected in duodenal - Size: 33-43 µm
aspirates or in sputum in heavy infection. - Covering: Thin outer transparent membrane
2. Culture: Not routinely done - Thick brown radially striated wall
3. Indirect evidence (embryophore surround the embryo)
a. Serology: - Within the egg there is a embryo with 3 pairs
of hooklets, the oncoshpere.
• Ab detection: By ELISA, Immunoblotting
Life cycle:
b. Blood examination:
i. Definitive host: Man → harbours the adult
• Peripheral blood eosinophilia
worm.
Taenia saginata ii. Intermediate host: Cattle (Cow/buffalos) →
♦ Common name: Beef tapeworm/unarmed tape worm. harbours larval stage.
♦ Habitat: Small intestine (Jejunum) Acquisition of infection by eating inadequately cooked
Morphology beef containing larval stage cysticercus bovis
Adult worm: ↓
- Length: 5 - 10 m Evagination of scolex and develops into adult worm in
small intestine and attain sexual maturity, fertilization
- Color: Whitish in color and semitransparent.
occur in segment and egg develop
- Largest helminth infecting man
↓
- It is divided into (i) Head (ii) Neck (iii) strobilla
Eggs are passed in feces after rupture of gravid
Head: segment
- Pear shaped, quadrate in cross section
V
↓
- Bear 4 circular sucker, no rostellum or hooks, Cow/buffalo ingest while grazing (human may be
so called unarmed tapeworm. infected by ingestion of vegetable or by water
Neck: contamination.
- Fairly long, fragile and narrower ↓
- Strobila: Strobila consists of 1000-2000 Reach systemic circulation by penetrating the gut
segments. The mature segments are 3-4 times wall and filtered in muscle tissues
longer as they are broad. ↓
- A mature segment contains male and female In muscle, the embryos develops into infective
reproductive organs. cystic larvae called cysticercus bovis
↓
- Testes are numerous
The cycle is repeated when human consume beef
- The gravid uterus consists of central
containing cysticerci bovis larva
longitudinal stem with 15-30 lateral branches
Cysticerus bovis
on each side of lobes.
- Is larval form (bladder form) of T. saginata
- Ovary → two - Develops in muscle of cow/buffalo
- Genital pore → situated marginally at the hind - It consist of 0.5-1cm diameter cyst containing a
end of each segment, alternating irregularly single invaginated scolex.
between right and left margin. - Is infective to man
- Gravid segment has vaginal sphincter. - Life span: 8 month (approximately)

Microbiology
Pathogenecity: • Gravid uterus: Consist of longitudinal

- Mode of infection: By ingestion of stem with 5-10 compound lateral
undercooked beef. branches on each side.
- Disease produced is called: Intestinal taeniasis • Ovary: Two with an accessory lobe.
(tape worm infection) which is characterized by: • Vaginal sphineter: Absent
abdominal discomfort, chronic indigestion, anemia, • Common genital opening: Mid-lateral
crawling segments rupture around perianal area. • Testes: 150-200
Laboratory diagnosis: Egg: Similar to T. sagniata (see T.sagniata)
A. Direct evidence Larva:
I. Examination of stool: to demonstrate gravid Cysticercus cellulosae:
segment and egg. - Measurement: 8 - 10mm and 5mm
II. Microscopy - The long axis of the cyst lies parallel with
a. Stool microscopy muscle fibre.
• Egg with characteristic thin shell and 6 - There is a dense milk-white spot at the side,
hooked on oncosphere are diagnostic. where scolex with its hooks and suckers
b. Segment microscopy remains invaginated.
• Applicable for the differentiate T. - The cyst contain a fluid rich in salt and
Saginata from T. solium albuminous material.
• Micro-examination of gravid segment - Life span: 8 months
pressed between two slide show 15-20 Life cycle:
lateral branch of uterus - Definitive host: Man
B. Serology - Inter mediate host: Pig, Occasionally man
- Used for detection of T. saginata coproantigen.
Note: Life cycle is similar to T. saginata except
- Serodiagnosis by IHA, ELISA intermediate host is pig and larval stage is cysticercus
V C. Diagnosis in animal cellulosae. See life cycle T saginata
- ELISA & CIEP using oncosphere as antigen have
been used with some success Pathogencity:
Mode of infection (MOI) (i) ingestion of uncooked
Taenia solium (05) pork (ii) Autoinfection
♦ Common name: Pork tapeworm or Armed tapeworm. Disease:
♦ Habitat: Small intestine (upper jejunum) - Taeniasis, cysticercosis, neurocysticercosis
Morphology: - Intestinal taeniasis
Adult worm: - Usually asymptomatic
- Length: 2-3 meter - Occasionally there may be abdominal pain with
- Life span: 25 yrs intestinal disturbances, anorexia, chronic
- Divided into (i) Scolex (ii) Neck (iii) Body indigestion, diarrohea, eosinophilia.
i. Scolex: Cysticercosis
• Measures 1mm diameter (pin head size) - It is fatal systemic condition
• Globular possess a rostellum with double - Caused by the cysticerci cellulosae living in
rows of hooklets and 4 circular suckers. human tissues.
ii. Neck: - The manifestations vary with number of
• Short, 5.1cmlong cysticerci and tissues and organs involved.
iii. Body/strobila: - Cysticercois is divided into
i. Subcutaneous type:
• Number: 800-900
• Usually found in head, limbs, neck abdomen.
• Measurement: 12mm × 6mm twice as
long as wide • Movable and painless

GIT
ii. Ocular type: B. Human cysticercosis

• Usually found in vitrous body or subretina a. Biopsy of subcutaneous nodules → show
• Visual disturbance often occur presence of suckers and hooklets on scolex.
• Dead worm may provokes local
b. Radiology: Calcified intramuscular cyst can be
inflammation causing blindness.
detected.
iii. Brain type (Neuro cysticerosis)
• Symptoms are: related to site of infection. c. Find needle aspiration cytology (FNAC)
• Manifested by headache, nausea, • Useful and cost effective since it eliminates
vomiting, epilepsy, mental disorder. the biopsy
• Epilepsy is most frequent symptom. d. Blood picture: Eosinophilia
Laboratory diagnosis: e. Serology: IHA,CFT, ELISA
A. Intestinal taeniasis
- Diagnosis is made by f. CT scans or MRI: Indicates presence of
a. Identification of gravid segmented in faeces cysticerci in brain
b. Detection of eggs in faeces.
Difference between T. sagniata & T. solium (06)
Feature T. Saginata T. Solium
1. Common name Beef tape worm/ unarmed tapeworm Pork tape-worm or armed tapeworm
2. Habitat Small intestine (jejunum) Small intestine (upper jejunum)
Morphology
1. Adult worm Tape like, 5-10m in length white, semi transparent Tape like, 2-3 meter in length white,
semi-transparent
2. Scoloex Quadrate with four sucker (pigmented) Globular pin head size with four
sucker. V
3. Head Head without rostellum and hooklets Head provided with rostellum armed
with double row of alternating large
and small hooklets
4. Neck Long, thin & fragile Short & thick, 5-6 mm long
Proglottides
1. Number 1000-2000 800-900
2. Size 20 × 5 mm 12 × 6 mm
3. Expelled Singly In chains of 5 or 6
4. Uterus Longitudinal stem with 15-30 lateral branches on Central longitudinal stem with 5-10
each side compound lateral branches on each side
5. Common genital Posteriorly, on lateral margin of each segment Mid lateral
opening
6. Testes 300-400 150-200
7. Life span 10 year 25 year
Larvae Cysticercus bovis Cysticercus cellulosae
Size 5-10 mm × 3.4mm 8-10mm ×5mm
Location Found in muscle of cow, buffalo Found in muscle of pig

Microbiology
Diphylobothrium latum II. Procercoid larva

♦ It is the longest parasite in the intestine of human • Elongated
being • 500-600µm long
Adult worm • Has 3 pair of hooklets
- Yellowish gray with central marking III. Plerocercoid larva
- Size: 3-10m in length • Glistening white, unsegmented with
- If has head/scolex, neck and strobilla wrinkled surface
Scolex • 1-2cm long with rudimentary scolex
- Spoon shaped - possess false grooves called • Remain in bent or twisted form.
bothria one on ventral & another on dorsal surface. Life cycle:
- No rostellum and hooklets - Definitive host: Human beings or other fish
Neck eating animals.
- Thin, unsegmented and longer than head. - Intermediate host: Need two intermediate
Strobilla host
- Consist of 3000-4000 segment i. First: Cyclops or diatoms
- Mature segment measure 2-4mm in length and ii. Second: Fresh water fish (trout, salmon etc)
10-20mm in breadth and has 3 genital opening Infection occurs by ingestion of raw or inadequately
on mid ventral aspect and opening are formed cooked fish containing plerocercoid larvae
as vas deferens, vagina and uterus in the order ↓
from front, on middle ventral surface. Plerocercoid larvae develop into adult worms in the
- Mature segment consist of bilobed ovary intestine of human beings
centrally coiled uterus. ↓
V Adult worms liberate eggs in lumen, which pass out
- After discharge of eggs through uterine pore,
with faeces of definitive host onto the soil and
dried up segment breaks off and is passed in
further eggs gain entry into water
chains in host's faeces.
↓
Egg:
Eggs develops in water forming coracidium - ciliated
- Shape: Oval embryo with 6 hooks (1st stage larva), which escapes
- Size: 70-45 µm from the egg through opercular end.
- Colour: Brown (bile stained) ↓
Coracidum is ingested by Cyclops and develops into
- Ovum: Unsegmented and surrounded by yolk
procercoid larva (2nd stage larva)
granules.
↓
- Operculated at one and have one knob at Infected Cyclops in swallowed by fish and
opposite side. plerocercoid (3rd stage larva) develops
- It doesn't float in saturated salt solutions. ↓
- Freshly passed eggs are not infective Human beings ingest plerocercoid larva in fish and
Larvae: cycle is repeated
I. Coracidium Pathogenecity:
• Spherical ciliated embryo - Disease produced by it is called Diphyllobothriasis
• 40-55 µm is diameter - Mode of infection: By ingestion of improperly
cooked infected fish or fish containing
• Has 3 pair of hooklets.
plerocercoid larvae.

GIT
- It causes: Eggs:
i. Gastrointestinal disturbances - Shape: Planoconvex →flattened on ventral
• Abdominal discomfort side and convex on dorsal side.
• Nausea, vomiting, diarrhea - Size: 50-60µ× 30µ

- Color: Colorless → non bile stained
• Loss of appetite and wt. loss
- Egg shell: Transparent
• Abdominal pain due to intestinal
- Ovum: Fully developed, a coiled tadpole like
blockage by worm
larva.
ii. Anemia by absorbing Vit. B12:
- Floats in saturated solution of common salt.
Bothriocephalus anaemia.
- Infective to man.
iii. Eosinophilia in early phase.
Life cycle:
Laboratory diagnosis
i. Macroscopic examination
- Intermediate host: Not required
a. Stool: for segments of adult worms
ii. Microscopic examination Egg with a tadpole like larva laid on perianal skin
iii. Serology: ELISA, latex agglutination completes its development in 24-36 hrs and becomes
mature
Enerobius vermicularis
↓
♦ Common: Pinworm, threadworm
Infection occur by ingestion of mature eggs
♦ Habitat: Caecum, vermiform appendix and
↓
adjacent parts of ascending colon.
Egg hatch in intestine to release the larvae
Morphology:
↓ V
Adult worm
The larvae develop into mature worms
- Shape: Small, white spindle - shaped, resemble
a piece of white thread. The male worm fertilizes the female worms & dies
- There are wing like expansions at the anterior ↓
end called cervical alae. The gravid female migrates out of the anus during
- No buccal cavity night and lays up to 10,000 on perianal skin
Male worm: ↓
- Measurement: 2 - 4 × 0.1× 0.2 mm The cycle, repeated
- The posterior end is curved and has a coiled tail Pathogenicity:
with a single spicule. - Mode of infection: Person to person by
- It dies after fertilization of the female. ingestion of eggs.
Female worm: - Disease caused by it: Enterobiasis
- Measurement: 8-13 × 0.3×0.5mm - It is common in children
- The posterior third of the body is pointed like a - Familial infection is common.
pin. So, called pin worm. - The egg deposited on perianal skin,
- Oviparous: mature female lays eggs and after contaminated night clothes and bed linens of
oviposition dies in 2 or 3 weeks. infected persons.

Microbiology
- Infection can be transmitted due to ♦ Habitat:

contamination of hands by handling night • In large intestine → in caecum and also in
clothes and bed linens. vermiform appendix.
- Autoinfection (Re-infection) is also possible in
Morphology
following way.
Adult worm:
i. By hand to mouth
- Shape: Pinkish white resembles a whip
ii. Retrograde infection:
- The anterior 3/4th is thin, hair like and coiled.
• The egg laid on perianal skin hatch out
- The posterior 2/5th is thick and stout →
into larvae, which migrate back through
the anus upto caecum and develop into resemble handle of whip.
adult worms. - The anterior portion contain a long capillary
Clinical features oesophagus
- Perianal pruritus and an eczematous condition - The posterior part contains the intestine and
around the anus and perineum reproductive organs.
- Nocturnal enuresis - It lives in intestine for many years.
- Inflammation of the vermiform appendix may Male worm:

also occur. - Length: 3-4 cm long
- Vulvovaginitis - The posterior end is coiled and has a single
- Salpingitis spicule.
- Pelvic or perineal granulosus rarely occurs. Female worm:

- Length: 4-5 cm long
V Laboratory diagnosis (04)
i. Enterobiasis should be suspected in children and - The posterior end is blunt and rounded.
adult who show perianal itching relieved only by - It is oviparous: Fertilized female lays eggs
vigorous scratching. 5,000 egg every day.
ii. Demonstration of adult worm Eggs:
- On the surface of stool sample - Shape:
- On the perianal skin • Barrel - shaped with projecting mucous
iii. Demonstration of eggs plug at both poles.
- As they are seldom excreted in faeces, stool - Size: 50µ × 25µ

sample is not useful for diagnosis. - Color: Brown → Bile stained
- So, diagnosis is made by collecting egg in - Egg shell: Double shell
morning sample collected from perianal skin by - Content:
adhesive pad cellophane tape/NIH (National • Unsegmented ovum which is not infective.
institute of Health, USA)
- It floats in saturated solution of common salt.
- Scotch tape swab
Life cycle
- Dirt from finger nails.
Trichuris trichura - Intermediate host: Not required
♦ Common name: Whipworm
GIT
Egg released in faeces, complete development occurs Laboratory diagnosis

slowly in water or damp earth I. Heavy infection
↓ Examination of stool: By saline preparation
Rhabditiform larvae develop in 3-4 weeks - Indicates characteristics Barrel - shaped, bile
↓ stained egg
Infection occurs by ingestion of embryonated egg - Adults may occasionally present.
with food or water II. In light infection
↓ - Concentration technique
Egg hatch in intestine to release the larvae, which - Routine wet mount of stool → for detection of
migrate to the caecum and appendix eggs.
↓ Eggs [06]
The larvae develop into adult worm. 1. Bile stained eggs
↓ i. Egg of A. lumbricoides
The anterior portion of adult worm lies embedded in ii. Egg of Trichuris trichuria
the mucous membrane and posterior end project in
iii. Egg of taenia species
the lumen
iv. Egg of Echinococcus granulosus
↓
2. Non bile stained egg
The mature sexually & fertilized female, lays eggs
which passes in faeces i. H. nana
ii. A. duodenale
↓
The cycle is repeated FOOD POISONING V
Pathogenecity: Definition:
- The diseased caused by it → Trichuriasis - Acute illness usually of sudden onset, brought
about by eating contaminated food poisonous
- Usually, worms donot produce any pathogenic
food like
effect.
• Bacteria or their toxins
- Light infection are asymptomatic
• Chemicals including metals
- Heavy infection
• Plants, fish, viruses, mycotoxins
Characterized by - It causes different clinical manifestations such as :
• Abdominal pain • Nausea and vomiting
• Bloody or mucoid diarrhoea • Abdominal cramps
• Wt. loss • Diarrhoea
- It may lead to: • Fever
• Anemia Note:
• Malnutrition - Food poisoning due to clostridium botulinum
• Growth retardation. causes constipation.
- Rarely, prolapsed of rectum in massive - Food poisoning associated with undercooked or
infection and appendicitis occur. raw seafood is due to vibrio parahaemolyticus.

Microbiology
Bacterial Food Poisoning

Incubation
Bacteria Source Mechanism of action Sign and symptoms
period
- Meat Heat stable enterotoxin - Vomiting, abdominal cramps,
1. Staphylo-
- Daily product 1-6 hours ingestion preformed in diarrhoea
cocus aureus
- Poultry food → GI symptoms - Last for 6 - 24 hours
Adsorb to epithelial cell
2. Salmonella - Raw meat - Chills fever, headache,
in small intestine → PMN
typhimurium, - Poultry of eggs 12-24 abdominal pain and profuse
and PG response → in
S. Cholerasuis - Raw unwashed hours watery diarrhoea
cAMP → watery
S. Enteritidis vegetable - Last for 2 - 5 days
diarrhea
- Reheated fried 2 different types of - Nausea, vomiting, abdominal
rice preformed enterotoxin cramps
3. Bacillus cereus 1-6 hours
- Meat, seafood, → one emetic form, - Last for less than 24 hours of
salad, potatoes other diarrhoeal form onset.
- Dysphagia, diplopia drooping
- Home canned eyelids
meat, vegetables
Preformed toxin → - Constipation
and fish
4. Clostridium 12-36 inhibit release of - Muscle weakness
- Pickle & home
botulinum hours acetylcholine in NM - Frequently fatal (1mg = 200
made cheese
junction million death) within 4-8 days
preserved at low
pH due to respiratory or cardiac
V failure.
Spores survive cooking
- Beef poultry, meat - Diarrhoea and abdominal
5. Clostridium → germinate → multiply
products 6-24 hours cramps
perfrigens rapidly between 30-50°C
- Reheated food - Nausea and vomiting rare
→ produce toxins
- Meat - Invasion →
- Diarrhoea, abdominal pain,
6. Campylo- - Poultry epithelium of small
2 - 11 days malaise: fever
bacter jejuni - Unpasteurized intestine
- Last for 2 - 7 days
milk - Heat stable toxin
- Meat, milk and - Abdominal cramps

Cytotoxin absorbed from
vegetables - Diarrhoea with blood
7. E-coli (EHEC) 3 - 8 days gut → damage vascular
contaminated by - Hemolytic uremic syndrome
endothelial cells
faeces - Can lead to death
- Milk
- Water Terminal ileum →- Fever
8. Yersinia contaminated enlargement of - Diarrhoea (frequently with
2-7 days
enterocolitis with wild, mesenteric lymph nodes blood and WBC)
domestic animals → necrosis - Abdominal pain
faeces.

GIT
Mycotic Poisoning • Amanita Virosa

♦ Poisoning due to the intake of fungus containing • Amanita versa
toxins. - Major toxins in mushroom are:
Mycotoxins: 1. Alpha amanitin
- Toxins formed by the hyphae of many fungi • Deadly
growing in contaminated foods and other
• Causes liver damage within 1 - 3 days of
substrate.
ingestion
- It causes mycotoxicosis which results from
• Principle toxin in Amanita
ingestion of food contaminated with
mycotoxins (fungal toxins). 2. Phallotoxin
Mycetismus: • Also found in Amanita
- Ingestion of toxins along with fungus • Causes GI upset
- Examples: 3. Muscarine
• Claviceps species – ergot poisoning • Sometimes deadly
• Coprine species – coprine poisoning • Acts as muscarine receptor against and
• Inocybe species – muscarine poisoning brings about different mucarinic symptoms
- Amanita species of mushroom most common • Death may occur due to respiratory failure
in poisoning are: 4. Ibotenic acid: Causes neurotoxicity
• Amanita phalloides (major)

Microbiology
SPECIAL POINTS FOR MCQs
Bacteriology:
Normal flora of GTI
1. The empty stomach is sterile due to gastric acid
2. But stomach may have scanty organism soon after eating.
3. In gastric carcinoma and pyloric stenosis, Gram positive cocci and bacilli proliferate in stomach
due to stagnation of food–stuff.
4. Normal flora increase progressively beyond duodenum to colon.
Part of intestine Bacterial count
i. Duodenum 103-106 per gram of content
ii. Jejunum and proximal ileum 105-108 per gram of content
iii. Lower ileum and caecum 108-1010 per gram of content
iv. Colon and rectum 1011-1013 per gram of content
5. The normal for a of adult colon contain 96-99% of anaerobes and only 1-4% aerobes. Bacteroides
(fragilis mainly) are predominant anaerobes followed by Bifidobacterium.
6. Anaerobic condition of colon is maintained by aerobes that utilize free oxygen. Enterococci are
predominant aerobes.
Clostridium difficle:
V 7. Causative agent of pseudomembranous enterocolitis (KU, 2013)
8. Is a normal gut commensal
9. Is Gram positive rod with oval and sub-terminal spore but has tendency to become Gram-
negative in old culture.
10. Noninvasive C. difficle produces 2 toxins
i. Enterotoxin (toxin-A) →produces symptoms
ii. Cytoxin (toxin-B → produces cytopathic effects.
11. Almost all antibiotics even the once used in treatment of pseudomembrane enterocolitis can cause
the disease.
12. Enterotoxin produced by C. difficle causes antibiotic associated pseudomembrane enterocolitis.
13. persons above 50 years of age are most susceptible to C. difficile infection.
14. C-difficle toxin is neutralized by C. Sordelli antitoxin.
15. Metronidazole is DOC
16. Vancomycin is also used
17. In severe cases, IV metronidazole is recommended
18. Cytotoxin say in stool is the best test.
Salmonella:
19. Are gram negative, motile bacilli
20. Have peritrichate flagella.

GIT
21. Need tryptophan as growth factor.

22. Selenite F is used as growth medium.
23. Affect payer’s patches in intestine.
24. H antigen is the most immunogenic.
25. Vi agglutination detects carrier.
26. Vi antigen is not seen in normal population
27. Blood culture is the gold standard for diagonosis
28. Diazo-reaction is also used of diagnosis
29. Causes 3 types of clinical syndrome human:
i. Enteric fever, ii. Septicaemia, iii. Gastroenteritis
Salmonella Species Diseases produces
S. typhi Typhoid fever
S. paratyphi A,B &C Paratyphoid fever
S. cholerae suis, S. paratyphic Septicaemia
S. typhimurium Food poisoning (Gastroenteritis)

30. Wilson and Blair bismuth sulphide medium is selective medium for salmonellae.
31. Jet black colonies with metallic sheen are formed due to formation of H2s.
32. S. typhi is anaerogienic, produces only acid and no gas.
33. Kauftmann – White scheme:- is diagnostic scheme based on ‘O’ & ‘H’ antigen identification by
agglutination test.
34. Enteric fever (Typhoid fever) is characterized by step-ladder pyrexia, relative bradycardia and rose spots. V
35. Rose spots is red macules , appear on chest and abdomen in 2nd and 3rd week.
36. Blood culture is very important specimen in first week of enteric fever.
37. In third week, widal test is best.
38. In fourth week, widal test(mainly) and stool and urine culture yields best result.
39. Stool culture is mainly done for detecting the carries.
Widal test: It is test of blood serum based on agglutination reaction to diagnose typhoid fever.
40. Presumptive serological test for enteric fever.
41. It is demonstration of agglutinating antibodies against antigen(in salmonella infection)
42. For brucellosis, only ‘O’ somatic Ag. Is used.
43. The antigen used in test the ‘H’ and ‘O’ antigen of S. typhi and H antigen of S. paratyphi.
44. The paratyphoid are not employed as they cross react with S. typhi ‘O’ due to variant of factor 12.
45. A single test of O titer of 1:100 or more and H titer of 1:200 or more is significant .
46. A rising titer of 4 fold or higher of 7-10 days is more meaningful than one test.
47. TAB vaccine →used for prophylaxis.
i. Is heat killed whole cell vaccine,
ii. Contain S. typhi 1000million + S. paratyphi A and B 750million/ml.
48. Live oral (Ty21a) is another typhoid vaccine.

Microbiology
Vibrio-Cholera:
49. 1st isolated by Robert Koch.
50. Most cases are subclinical.
51. Gram-negative nonsporing, non capsulated curved or comma shaped bacilli.
52. Very actively motile with a single polar flagellum.
53. The movement is of darting type Darting Motility.
54. Slective Medium for V. Cholera.
i. TCBS (Thiosulphate .Citrate Bile Sucrose agar)
ii. BSA(Alkaline Bile Salt agar)
55. Transport Medium.
i. Venkataraman-Ramakrishan (V.R) medium
ii. Cary –Blair medium.
56. Toxin action is CAMP mediated
57. Humans are the reservoir
58. Survive boiling for 30 seconds and cold temperature (ice for 4-6 weeks)
59. Causes Rice water stools/Pea soup diarrhea.
60. Non halophilic.
61. V. cholera has 2 biotype→classical and EI. tor.
62. V. cholera has 3 serotypes (1) Ogawa(AB) Inaba (AC) and Hikojima (ABC) on the basis of minor ‘O’
antigens.
63. Non-01 V. cholera is K/A →Non –agglutinating vibrios (NAG)
V Escherichia Coli:
64. E. coli, kleb. , serratia,citrobacter porteus,morganella belong to Enterobacteriaciea.
65. E. coli, klebsiella, Enterobacter are Lactose fermenter.
66. Salmonella, shigella, proteus, pseudomonas→Non lactose fermenter.
67. Gram negative, non-sporing , non-capsulated.
68. Is divided into six pathotypes,of intestinal pathogens. which are:
i. Enterotoxigenic E. coli (ETEC) →commonest causes for Traveller’s diarrhea.
ii. Enterohemorrhagic E. coli (EHEC) →Also called Shiga like toxin producing E. coli.
→ Shiga like toxin also called →Verotoxin.
iii. Enteropathogenic E. coli (EPEC) →Important cause of Infant diarrhea.
iv. Enteroinvasive E. coli (EIEC)
→ Shares may feature with shigella infection
→ Unlike shigella. EIEC causes disease only at high inoculums(108to 1010CFU
→ Penetrate Hela cells in tissue culture.
v. Enteroaggregative E. coli (EAEC)
vi. Primarily found in developing countries and mostly affect young children.
vii In vitro, the organism exhibit a diffuse or stacked –brick” adherence pattern.
69. Toxins produced by E. coli are
i. Enterotoxin, ii. Hemolysin, iii. Vero cytotoxin.
GIT
70. Nephrotoxigenics strain of E. coli are 09, 02, 04, 06, 07, 018, and 075.
71. Most strains of Eschaerichia are motile due to peritrichate flagella.
72. E. blattae→non motile
73. Enterotoxigenic E. coli (ETEC) produce one or both of two enterotoxins, a heat-labile toxin (LT)
and a heat-stable toxin(ST).
Shigella:
74. Gram-negative, aerobic, non-motile, non flagallete, non capsulated
75. Non Lactose fermenter.
76. S. sonnei is late lactose fermenter.
77. Ferment mannitol ,except S. dysentriae.
78. Most virulent type is S. dysenteriae.
79. Stool culture is best test.
80. Subdivided on the basis of Mannitol fermentation.
81. In shigella-Salmonella agar, the colonies of shigella are colourless.
82. Causes superficial snail. Tract of serpiginous ulcers.
Helicobacter Pylori:
83. Is a Gram-negative, spiral flagellate bacillus,
84. Non Invasive, lives Gastric mucus.
85. Its spiral shape, flagellae render H. pylori motile in the mucus environment.
86. Its efficient urease protects it against by catalyzing urea hydrolysis to produce buttering ammonia.
87. In vitro , H. pylori is microaerophilic and slow- growing and requires complex growth media.
88. Complete genomic sequence has been studied. V
89. Causes duodenal ulcer (stronger relation) and gastric ulcers.
90. Transmitted from man to man, feco-orally and orogastric route.
91. The test of choice for documenting eradication is the urea breath test (UBT).
92. Rapid urease test is most rapid and dependable test for defection of H. pylori.
93. Urea breath test:- Isotope of carbon(C14) is fed to patient.
94. Urine test :- Isotope of nitrogen-15 N15 is used as urea.
Campylobacter:
95. Are motile
96. Non-spore-forming
97. Curved gram-negative rods,
98. Microaerophilic
99. The principal pathogen is C. Jejuni
100. Skirrows medium is culture medium
101. Butzlers medium is culture medium
Food Poisoning:
102. Food kept at 50c-630c has active bacterial multiplication, so intake of such food is the danger.
103. E. coli 0157 causes food poisoning.
104. Aflatoxin is produced by Aspergillus flavus and parasiticus

Microbiology
105. Aflatoxin B1 is highly carcinogenic and widespread occurrence in foods.

106. Ochatoxins is produced by A. ochraceus, which is a nephrotoxin.
107. Fusarium species produces
i. Trichothecenes, ii. Zearalerone
108. Patulin is produced by penicillium, Aspergillus
109. Alternaria-tenuazonic acid→detected in commercial tomato paste.
110. Amanita phalloides→Major cause of mushroom poisoning
111. Major mushroom toxins are α−amanitin, phallotoxin, muscarine and ibotenic acid
112. Ibotenic acid causes neurotoxicity.
113. Food poisoning due to reheated rice is due to Bacillus cereus.
114. In food poisoning due to clostridium botulinum , constipition occurs not diarrhoea.
Parasitology:
Giardia Lambia
1. It is bilaterally symmetrical protozoan.
2. Trophozoite has 2 axostyl, 2 nuclei and 4 pairs of flagella.
3. Cyst has 4 nuclei which may remains of the flagella and the margins of sucking disc.
4. Acid environment causes the parasite to encyst.
5. Cyst is bile stained.
6. G. lambia doesnot causes invasion of tissue but causes intestinal disturbance leading to
malabsorption of fat i.e. steatorrhoea.
7. It does not cause bloody diarrhoea with mucus.
V 8. Trophozoite show slow oscillation motility along its long axis, which is comparable to falling leaf.
9. It divides by longitudinal binary fission.
10. Mode of transmission is few oral route.
11. In heavy infection, it causes disaccharidase deficiency leads to lactose intolerance that undergoes
resolution after treatment.
12. Giardia lambia attaches to small intestine mucosa with sucking disc.
Balantidium coli:
13. Definitive host - pig, man is accidental host
14. No intermediate host
15. Infection form: Binucleate cyst
16. Clinical disease is manifested when trophozoite eroide intestional mucosa unlike G. lambia
17. It causes mucosal ulcer and submucosal abscess.
Entamoeba histolytica:
18. Infection stage: Mature cyst (Quadrinueleate) or cyst.
19. About 90% of infection are asymptomatic, but remaining 10% produce a spectrum of clinical
syndromes ranging from dysentery to abscesses of liver or other organs.
20. Both trophozoite and cyst are found in the intestinal lumen, but only one trophozoites of E.
hisotolytica invade tissue.
21. Cyst has glycogen mass, chromoidal bar, eccentric nucleus.

GIT
22. The most common type of amoebic infection is asymptomatic cyst passage.
23. Amoebic liver abscess is an extra intestinal infection by E. histolytica.
24. Pleuropulmonary involvement (20%-30% of patients), is the most frequent complication of
amoebic liver abscess.
25. Primary amoebic encephalitis is caused by → Nagleria flowerie
26. Fulminant amoebic meningoencephalitis is cause by Nagleria flowerie
27. Granulomatous amoebic enceptialitis is caused by → Balmuthia mandralliy.
28. VIrulence is related to secretion of potent cysteine proteinase.
29. Cystein proteinase produced by invasive strains of E. histolytica inactivates complement factor
(C3) and thus resistant to complement mediated lysis.
30. Cystein protein cleaves ECM, fibtonectin, laminin and Type - I collagen.
31. Best way to distinguish amoebic liver abscess from bacterial liver abscess in serological evidence of
E. histolytica.
32. E. Histlytica can be cultivated in
i. Boeck and Drhohalv's medium ii. Diamond's axenic medium
iii. Balamutub's medium
33. E. histolytica multiplies by Binary fission
34. Bundle of crystalline ribonucleic acid is called chromatoidal bodies.
35. Pathogenic E.histoloytica strains are best distinguished from non pathogenic strains by Isoenzyme
analysis.
36. Anchovy sauce 'pus' of amoebic liver abscess is mainly contributed by Degenerated nepatocytees.
37. Nagleria fowleri infection is usually transmitted by swimming.
38. Charcot - leyden crystals are derivative of Eosinophils.
V
39. Isospora belli is only protozoan which is consistently associated with eosinophilia.
40. Pentamidine isethionate is used to prevent pneumonia due to pneumocystis carini in AIDS patients.
Worms (Heminthology):
41. Common names of parasites:
Tape worm Worm/ Parasites Common names
- Diphyllobotherium → Fish tapeworm
- Taenia saginata → Beef tapeworm
- T. solium → Pork tapeworm
- H. nana → Dwarf tapeworm
- H. diminuta → Raw tapeworm
- E. granulosus → Dog tapeworm
- Clonorchis sinesis → Chinese liver fluke
- Fasciola hepatica → Sheep liver fluke
- Fasciola buski → Giant intestinal fluke
- Paragonimus westermanii → Lung fluke
- E. Granulosus → Hydatid cyst
- E. mutilocularis → Alveolar hydatid

Microbiology
42. Parasites causing autoinfection

i. T. solium ii. S. stercotralis
iii. H.nana iv. E. vermicularis
v. Cryptosppridium parvum vi. Capillaria philippinensis
43.
Parasites Infective form Transmission
A. Lumbricoides Embryonated egg Ingestion
E. vermicularis Embryonated egg Ingestion
S. stercoralis Filariform larva Penetration of skin
T. trichiuris Embryonated egg Ingestion
A. duodenale Filariform larva Penetration of skin
N. americana Filarifom larva Penetration of skin
44. Bile stained egg
i. Egg of A.lumblicoides ii. Egg of Trichuris trichura
iii. Egg of taenia species iv. Egg of Echinococcus granulosus
45. Non bile stained egg
i. H.nana ii. A.duodenale
Ascaris lumbricoides:
46. Because of its resemblance to earth wrom(Lumbricus teres), the name for common earthworms.
The parasite is called Ascaris lumbricoides.
V 47. The parasite maintain position by muscle tone and show spinal movement.
48. Female is larger than male.
49. Has two types of egg liberated (i) fertilized (ii) unfertilized egg both are bile stained.
50. Infective form: Embryonated egg.
51. The larva of A. lumbricoides undergoes 4 times moulting.
One → outside, two in lung, and last in (4th) in intestine.
52. Ascariasis in pregnancy should be treated in 1st trimester.
53. Egg becomes infective in 21 days after passing in stool.
A. Duodenale:
54. Female adult worm is larger than male worm.
55. Adult worm looks reddish brown due to ingested blood.
56. Eggs are laid in an unsegmented stage during their passage through the bowel. It become of 4
celled stage i.e.4 blastomere.
57. Egg is non bile stained.
58. No intermediate host is required.
59. It is also called old world hookworm.
60. Larva undergoes 4 moulting.
1st and 2nd moulting → in soil
3rd moulting → in oesophagus.
4th moulting in → small intestine

GIT
61. Mode of infection is: By penetration of skin.

62. Infective form → 3rd stage filariform larva.
63. Anemia is most chronic clinical manifestation manifested by it.
64. N. americanus is new world hookworm.
65. N. americanus is less pathogenic to A.duodenale.
66. For further information: Refer text
Strongyloides stercoralis:
67. Smallest nematode inhabits in upper part of small intestine.
68. Only female adult worm is demonstrated in human.
69. Female adult worm → ovo viviparous.
70. Has two larvae
i. Rhabditiform → Activiely motile, double bulb oesophagus.
ii. Filariform → Infective form has cylindrical oesophagus.
71. It causes internal autoinfection.
72. In immunocopromised patients, it causes hyper infection syndrome and disseminated
strongyloidosis.
T. Saginata:
73. Called beef tapeworm/ unarmed tapeworm.
74. Strobilla consist of 1000-2000 proglottids
75. Has two ovary
76. Testes: 300-400
77. Egg: bile stained V
78. Larvae: Cysticerus bovis → life span 8 month.
79. Mode of infection: Ingestion of under cooked beef.
80. Definitive host: Man
81. Intermediate: Cattle (Cow, buffalo)
T. Solium
82. Pork tape wrom /armed tapeworm
83. Strobilla: 800-900 proglottids
84. Testes: 150-200
85. No vaginal aphineter.
86. Same egg as that of T. saginata.
87. Larvae: Cysticercus cellulosae.
88. Definitive host: Man
Intermediate host: Pigs
89. Cuases subsutaneous cysticerosis
Ocular cysticercosis
Neuro cysticercosis
90. Causes Auto infection

Microbiology
D. Latum:
91. K/A → Fish tapeworm
92. Liver in small intestine
93. Longest intestinal parasite of man
94. Bile stained operculated egg (not infective to man)
95. Human → definitive host
96. Infective stage for man: plerocercoid larva from fish.
97. Inhibits dietary absorption of vitamin B12, So can cause megaloblastic anemia.
98. Length of parasite: 10 meter
Enterobius vermicularis:
99. Commonly called → pinworm, thread worm
100. Has not buccal cavity but has cervical alae.
101. Female oviparous
102. Male dies after fertilized the female.
103. Egg-non bile stained and contain a coil tadpole like larvae.
104. Causes autoinfection, retrograde infection
105. Diagnosed by cellophane tape
Trichuris trichuria:
106. Commonly called whipworm.
107. Adult worm → within resemble a whip
108. Eggs → Bile stained, barrel shaped with a projecting mucous plug at each pole.
V 109. Infection by ingestion of embryonated egg.
110. After ingestion of egg, it hatches in small intestine but there is no migratory phase.
Rota - virus
111. Rota virus is non cultiviable virus
112. Main cause of infantanile diarrhoea.
113. Causes destruction of mature enterocytes.
114. Double walled, wheel like appearance in electron microscope.
115. "SPLIT GENOME" is feature of rota virus.
Norwalk virus:
116. Causes epidemic viral gastroenteritis in adults.

GIT
Pathology
SYLLABUS
Oral Pathology- premalignant Lesions: (p. 119)
List, morphology
Squamous Cell Carcinoma: (p. 119)
Aetiopathology, morphology
Pleomorphic Adenoma: (p. 120)
Classification, gross and morphology of pleomorphic adenoma.
Barret's oesophagus (p. 121)
Carcinoma of the Oesophagus: (p. 122)
Aetiopathogenesis, gross and microscopic features.
Peptic Ulcer: (p. 122)
Definition and sites of occurrences, pathogenesis, gross and microscopic features and complications.
Carcinoma of the Stomach: (p. 125)
Benign and malignant; Classification; aetiopathogenesis, gross and microscopic features
Tuberculosis of Intestine: (p. 126)
Pathogenesis, gross and microscopic features, complications.
Typhoid of Intestine: (p. 127)
V
Appendicitis: (p. 127)
Amoebic Colitis: (p. 128)
Aetiology, gross and microscopic features, complications.
Necrotizing enterocolitis: (p. 129)
Pathogenesis and morphology
Ulcerative Colitis and Crohn's Diseases: (p. 129)
Aetiology, gross and microscopic features, complications.
Polyps of large Intestine: (p. 133)
Classification, comparison of morphology of tubular and villous adenomas
Carcinoma of the Colon: (p. 131)
Pathogenesis, gross and microscopic features.
Acute pancreatitis: (p. 134)
Aetiopathogenesis, morphology and complications.
Carcinoma of the pancreas: (p. 135)
Morphology and complications.

Pathology

GIT
PATHOLOGY
ORAL PATHOLOGY Histologically:

Premalignant lesions - Superficial erosions with dysplasia, carcinoma
insitu or already developed carcinoma in
1. Leukoplakia
surrounding margins
2. Erythroplakia
- Subepithelial inflammatory infiltration
3. Speckled leukoerythroplakia
- Vascular dilation
Leukoplakia: Speckled leukoerythroplakia:
- "A white patch or plaque that cannot be - Characteristics of Both leukoplakia and
scraped off and cannot be characterized erythroplakia
clinically or pathologically as any other disease"
Note:
Note: If a white lesion in oral cavity can be given a
- All leukoplakias must be considered precancerous
specific diagnosis, it is not leukoplakia. So, white
until it is proved otherwise via histological
patches caused by entities such as lichen planus and
evaluation.
candidiasis are not leukoplakias.
- Premalignant changes may be seen in adult at any
Morphology: age but usually between ages 40 and 70.
Site: - Male: female occurrence = 2:1
- Buccal mucosa - Etiology: Tobacco use.
- Floor of mouth Alcohol, spicy foods, jagged teeth, ill fitting
- Ventral surface of tongue, palate and gingival dentures. V
or, anywhere in oral cavity
Gross: SQUAMOUS CELL CARCINOMA OF
- Solitary or multiple white patches or plaques. ORAL CAVITY
- Sharply demarcated borders. ♦ Among of head and neck, 95% occurs in oral
cavity.
- Lightly thickened, wrinkled, fissured or smooth.
Etiopathogenesis:
- May appear raised, corrugated, verrucous
plaques. Strong association:
Microscopy: - Tobacco smoking/Chewing.
- Hyperkeratosis. - Chronic alcohol abuse
- Dysplastic changes. - HPV 16, 18, 33
- Sometimes carcinoma insitu. Weak association:
- Lymphocytic infiltration - Chronic irritation (jagged teeth, ill fitting
dentures)
Erythroplakia:
- Submucosal fibrosis
- A red, velvety, possibly eroded area within the
oral cavity - Poor nutrition.
- Usually remains in level with or may be slightly - Actinic radiation

depressed in relation to surrounding mucosa. - Plummer - Vinson syndrome.

Pathology
Molecular biology: PLEOMORPHIC ADENOMA

- Activation of oncogenes Classification of tumors of salivary
- Inactivation of tumor suppressor genes. gland
Morphology: Histological classification:
Sites:
Benign Malignant
- Ventral surface of tongue, floor of mouth,
- Pleomorphic - Mucoepidermoid
lower lip, soft palate, gingival
adenoma/mixed carcinoma (15%)
Gross:
( 50%)
- Early stages, possibly mistaken for leukoplakia.
- Warthin tumor - Adenocarcinoma (10%)
Types: (5- 10%)
1. Ulcerative: Ulcerated protruding mass,
- Oncocytoma (1%) - Acinic cell carcinoma (5%)
Irregular and indurated borders
2. Papillary/verrucous type: Soft, wart like, - Other adenomas - Adenoid cystic carcinoma
(5% to 10%) (5%)
growth
3. Nodular type: Firm, slow growing, - Basal cell adenoma - Malignant mixed tumor
submucosal nodule. (3-5%)
4. Scirrhous types: Infiltration into deeper - Canalicular - Squamous cell carcinoma

structures. adenoma (1%)
• Cervical LN involvement. - Ductal papilloma - Other carcinoma (2%)
V Note:
@ PWOO BCD @ MAAAMS
i. Most common sites of distant metastasis:
- Mediastinal lymphnodes, Lungs, Liver and
Note: Carcinoma arising in pleomorphic adenoma is
bones
referred to variously as a "Carcinoma ex pleomorphic
ii. Site of local metastasis → cervical lymphnodes adenoma" or malignant mixed tumor.
Microscopy: Pleomorphic adenoma:
- Dysplastic lesions ♦ 60% of tumors in parotid gland.
- May or may not progress to full thickness ♦ Are less common in submandibular glands and
prior to invasion rare in minor salivary glands.
- Ranges from well differentiated keratinising Morphology:
neoplasm to Anaplastic semisarcomatoid
Gross:
tumors.
- Rounded, well demarcated masses, < 6cm
Note: - Encapsulated but expansile growth produces
- In cervical cancer: full thickness invasion occurs tongue like protrusion into surrounding gland.
prior to invasion - Cut surface:
- Relative degree of keratinization is not related • Gray-white with myxoid and blue
with behavior. translucent chondroid area.

GIT
Microscopy: BARRET'SOESOPHAGUS
- Posses both epithelial and mesenchymal Past Questions:
component 1. Short notes on Barret’s oesophagus [10 Jan]
1. Epithelial component: ♦ Complication of chronic GERD that is
• Epithelial elements resembling ductal characterized by intestinal metaplasia within the
cells or myoepithellal cells are present. esophageal squamous mucosa
• These cells are arranged in duct ♦ It confers increased risk of esophageal
formations, acini, irregular tubules, adenocarcinoma
strands or sheets of cells. ♦ Sequence of progression is:
• These cells are dispersed within Barrets epithelium
mesenchyme like background. ↓
2. Mesenchymal component (product of Dysplasia
myoepithelial cells): ↓
• Islands of chondroid tissue and rarely Carcinoma insitu
foci of bone. ↓
• Simulates cartilage Invasive adenocarcinoma
♦ Pathogenesis:
- Unclear, appears to result from alteration in
differentiation of stem cells of esophageal mucosa.
Morphology:
Gross:
- One or several tongues or patches of red
velvety mucosa extentending upward from V
gastroesophageal junction.
- Metaplastic mucosa alternates with residual
smooth, pale squamous mucosa
- Long segment barret's esophagus → in which 3
cm or more involved.
- Short segment → If less than 3 cm involved.
Microscopy:
1. Intestinal metaplasia:
• Contains: Gastric glands, Intestinal
epithelium with goblet cells, inflammatory
infiltrates, Dysplastic changes
Clinical Features:
• Dysplasia may be:
- Painless, slow growing, mobile discrete mass
within parotid, submandibular or buccal Low grade High grade
glands. - ↑ed epithelial proliferation - More severe
- Recurrence after surgery because of - Atypical mitoses cytological
incomplete removal: - Nuclear hyperchromasia & and
stratification architectural
1. Proximity to facial nerve
changes
2. Multiple foci of tumor - Irregularly clumped chromatin
3. Pseudoencapsulation. - ↑ N/C ratio

Pathology
CARCINOMA OF ESOPHAGUS PEPTIC ULCER

Squamous cell carcinoma: Past Questions:
♦ Most common carcinoma in esophagus.
1. Define peptic ulcer. List the sites of occurrence and
♦ Male: female = 2 -20:1
discuss its pathogenesis. Enumerate the complication
Etiopathogenesis:
1. Dietary factors: of peptic ulcer. (1 +2 +5 +2 = 10) [09 July]
- Deficiency of Vitamin A, C, B1, B6 2. Describe the etiopathogenesis, gross and
- Deficiency of trace elements: Zn, Mb microscopic feature and complications of peptic
- Fungal contamination of food stuffs. ulcer. (3 +5 +2 =10) [08 Jan]
- High nitrite/Nitrosamine 3. Define peptic ulcer. Describe aetiopathogenesis.,
- Betel chewing gross and microscopic features of peptic ulcer. Name
2. Life style the various complications. (2 +6 + 2 = 10) [07 July]
- Hot beverage, food
4. Describe the etiopathogenesis, gross and
- Alcohol consumption
microscopic features and complications of peptic
- Tobacco use
- Urban environment. ulcer. (4 +4 +2 = 10) [07 Dec, 06 Dec]
3. Esophageal disorders: 5. Define peptic ulcer. Explain its aetiopathogenesis
- Long standing esophagitis. and complications. (2 +6 +2 = 10) [05 Dec]
- Ectodermal dysplasia ♦ Chronic, most often solitary lesions that occur in
- Achlasia any part of GI tract exposed to aggressive action
- Plummer Vinson syndrome of acid/peptic juices.
4. Genetic predisposition:
Sites of Occurrence [09]
- Loss of tumor suppressor genes: P53, P16, INK
V 4a. In descending order of frequency:
Morphology: 1. First part of duodenum
Gross: 2. Stomach, usually antrum
- Site:
• Middle 2/3rd (50%) 3. Gastroesophageal junction, in setting of
• Lower 1/3rd (30%) gastroesophageal reflux or Barrett esophagus.
• Upper 1/3rd (20%) 4. Within the margins of gastro jejunostomy.
- Early lesions: Small, gray - white, plaque like 5. In duodenum, stomach and or jejunum of
thickening.
patients of zollinger Ellison syndrome.
- Over month to years: Polyploid/ exophytic/
protruded (60%), Flat (15%), ulcerated (25%) 6. Within or adjacent to meckels diverticulum
Microscopy: that contains ectopic gastric mucosa.
- Moderate to well differentiated
Note: 4 times more common in proximal duodenum
- Several histological patterns: verrucous,
spindle cells, basaloid. than in stomach.
- Individual cell keratinisation and intercellular Pathogenesis: [05, 06, 07, 08, 09]
bridges called desmosomes are seen.
- Prickle cells, keratin formation, epithelial keratin Cause:
pearls formation, undifferentiated forms. - Imbalance between gastroduodenal mucosal
Note: Adenocarcinoma usually occur in distal third of defense mechanism and damaging forces.
esophagus.

GIT
Note: 5. Bacterial PAF promotes thrombotic occlusion of V

Role of H pylori: surface capillaries.
6. Bacterial Ag recruits inflammatory cells to the
1. - Induces intense inflammatory and immune
response causing increased production of pro- mucosa.
inflammatory cytokines such as IL - 1, IL- 6, TNF 7. Damage to mucosa permits leakage of Nutrients
and most notably IL - 8 into surface microenvironment, thereby sustaining
- Secretes urease that converts urea into the bacillus.
ammonia, Ammonia thus released forms Role of NSAIDS:
ammonium chloride with the help of chloride
salts 1. ↓ PGs→ direct chemical irritation by cigarettes
and Alcohol → ↓ Blood flow and healing.
↓
Myeloperoxidase from Neutrophils elaborates Gastric hyperacidity occurs during:
monochloramines from these compounds 1. Zollinger Ellison syndrome
which causes gastric injury. 1. Ca++ associated i.e. renal failure, hyperparathyroidism
2. Elaborates enzyme phospholipase → damages
surface epithelium. Morphology: [06, 08]
Gross:
3. Proteases, phospholipase → Break glycoprotein -
- Round to oval, sharply punched out defect
lipid complex in mucus → No first line defense
with relatively straight walls.
mechanism.
- Margins are generally in level with surrounding
4. ↑ Acid and↓ HCO3– secretion.
mucosa or slightly elevated.

Pathology
- Depth may vary; superficial lesions extend till Features Benign Ulcer Malignant Ulcer
mucosa while deep excavated ulcers have base 1. Age Younger age Older age
in muscularis propria. 2. Sex Markedly Slightly common
- Base is smooth and clean owing to peptic common in in males
digestion of exudate. males
- Base of ulcer may have thrombosed or even 3. Duration of Weeks to years Weeks to
patent blood vessels. symptoms months
- Surrounding mucosa creates mucosal folds 4. Location Commonly lesser Commonly
radiating from crater in a spoke like fashion. curvature of greater curvature
pylorus and of pylorus &
Note: antrum antrum
- Peptic ulcers are solitary in more than 80% patient 5. Gross
- Lesions < 0. 3cm diameter tend to be shallow features
- Lesions > 0.6 cm are likely to be deep ulcers. a. Size Small Large
b. Shape Regular Irregular
c. Mucosal Radiating Interrupted
folds
d. Ulcer bed Haemorrhagic Necrotic
6. Barium Punched out Irregular filling
studies ulcer defect
7. Acidity Usually normal- May be normal-
to - low to-even
achlorhydria
V 8. Therapy Responds well to Usually does not
medical therapy respond to
medical therapy
Complications [05, 07, 08, 09]
1. Bleeding:
- Most common complication (MCQ 2013 KU)
- Occurs in 15-30% patients.
- Accounts for 25% of ulcer deaths.
Microscopy: - Life threatening
4 Distinct zones
- May be first indication of ulcer.
- Base and margin have a superficial thin layer of
2. Perforation:
necrotic fibrinoid debris.
- Occurs in 5% of patients.
- Beneath the necrotic layer lies zone of non
specific inflammatory infiltrate with neutrophils - Accounts for 2/3rd of ulcer death.
predominantly. - Rarely presents first indication of ulcer.
- In deeper layers, especially in the base of ulcer, 3. Obstruction due to edema or scarring:
there is active granulation tissue infiltrated - In 2% patients
with mononuclear leucocytes. - Most often due to pyloric ulcers, also with
- Granulation tissue rests on a more solid fibrous duodenal ulcer.
or collagenous scar. - Cause incapacitating, cramp like, abdominal pain.
GIT
CARCINOMA OF STOMACH 2. Environmental factors:

Past Questions: a. Diet:
1. Describe the aetiopathogenesis, gross and • Nitrites (Water, preserved food)
microscopic features of carcinoma stomach. • Smoked and salted foods, pickled
(4+2+4=10) [01 Dec] vegetables, chili
2. Discuss the aetiopathogenesis, classification, • Lack of fresh fruit and vegetables.
gross and microscopic features of carcinoma • Consumption of dietary carcinogens like
stomach. (3+3+2+2=10) [02 June] benzopyrene, N - nitrosocompounds.
3. Early gastric carcinoma [06 Dec] b. Low socioeconomic status.
c. Cigarette smoking
WHO Classification [02]
3. Host factors:
1. Epithelial tumors:
- Chronic gastritis (Hypochlorhydria, intestinal
- Intraepithelial neoplasia: Adenoma
metaplasia)
- Adenocarcinoma
- Partial gastrectomy (favours efflux of bile,
• Papillary alkaline food)
• Tubular - Gastric adenoma.
• Tubulopapillary - Barrett esophagus (tumor of gastroesophageal
• Mucinous junction)
• Signet ring 4. Genetic factors:
• Undifferentiated - Blood groups A are at high risk
• Adenosquamous - Family history increases likelihood.
- Small cell carcinoma
- Hereditary non-polyposis colon cancer syndrome.
- Carcinoid tumor.
- Familial gastric carcinoma syndrome (e-cadherin
2. Non epithelial tumors:
mutation) V
- Leiomyoma
- Schwannoma Types
- Granular cell tumor 1. On the basis of depth of invasion:
- Leiomyosarcoma a. Expanding (confined to mucosa and submucosa)
- GI stromal tumor b. Infiltrating (extends below submucosa)
- Kaposis sarcoma 2. Macroscopic subtypes:
- Others a. Early: Exophytic, flat/depressed, excavated.
3. Malignant Lymphoma b. Advanced: Ulcerative, fungating (polypoid)
Lauren classification scirrhous (linitis plastica), colloid (mucoid)
♦ Intestinal type, diffuse type 3. Histologic subtypes
Etiopathogenesis [01, 02] a. Intestinal type
- Tubular
Risk factors:
- Papillary
1. H-pylori infection:
- Tubulopapillary
- ↑ed risk 5-6 fold in intestinal type.
- Mucinous
- Inflammation → chronic gastritis → Atrophy →
- Adenosquamous
Intestinal metaplasia → Dysplasia → carcinoma.
- Undifferentiated.
- Long standing mucosal inflammation:
b. Diffuse type:
hypochlorhydria, ↓ pepsin secretion.
- Signet ring.

Pathology
Morphology [01, 02] TUBERCULOSIS OF INTESTINE

A. Location Pathogenesis
- Pylorus and antrum: 50-60% TB of intestine can occur in 3 forms:
- Cardia: 25% Hyperplastic
- Body and fundus: Rest Primary Secondary caecal
Note: Lesser curvature is involved more than greater tuberculosis
curvature. - Due to ingestion - Swallowing - Variant of
of contaminated of coughed occurring
B. Depth of invasion:
milk up infective secondary to
- Early gastric carcinoma: Confined to mucosa
material pulmonary - TB
and submucosa.
- Advanced gastric carcinoma: extends beyond
sub mucosa into muscular coat. Organisms are seed to mucosal lymphoid aggregates
of small and large bowel.
C. Macroscopic patterns:
a. Exophytic: Protrusion of tumor mass into ↓
lumen. Undergo granulomatous inflammation
b. Flat or depressed: No obvious tumor mass ↓
within the mucosa. Advanced cases with flat Lead to ulceration of overlying mucosa
surface → Linitis plastica or leather bottle
Morphology Gross Microscopy
appearance
c. Excavated: Shallow or deep erosive crater Primary - Affected - Initially there is
present in the wall. In advanced cases, craters Intestinal lymphnodes primary complex of
are indentified by their heaped up, beaded TB enlarged, Ghon's focus.
V margins and necrotic base with neoplastic matted and - Typical tubercular
tissue extending to surrounding mucosa and caseous. granulomatous
walls. - Healing by inflammatory
D. Histological patterns: fibrosis and reaction with
Intestinal type calcification casseous necrosis
- Malignant glands, abundant mucin in lumen. Secondary - Ulcers which - Initially there is
- Intestinal metaplasia Intestinal are transverse primary complex
- Desmoplasia TB to long axis of or ghons focus
- Neoplastic cells with apical mucin. the bowel - Typical tubercular
Diffuse type: - May be coated granulomatous
- Gastric type mucous cells but don't form glands with caseous inflammatory
- Mucin formation which expand the malignant material reaction with
cells and push the nucleus to periphery → i.e. - Serosa studded casseous necrosis.
signet ring like cells. with visible - Granulomatous
E. Metastasis: tubercles. inflammatory
- Supraclavicular sentinal node: Virchow node - Transverse reaction with
fibrous central caseation
- To periumbilical region forming subcutaneous
nodule called as sister Mary Joseph nodule. strictures and - Mucosa and
intestinal submucosa show
- Local invasion to duodenum, pancreas,
obstruction in ulceration
retroperitonueum.
advanced cases
- Bilateral metastasis to ovary: Krukenberg tumor.

GIT
TYPHOID OF INTESTINE APPENDICITIS

Pathogenesis Past Questions:
Typhoid bacillus ingested through contaminated food 1. Give pathogenesis of this lesion. [3][PBQs 2013]
or water.
Etiopathogenesis [PBQs 2013]
↓
Etiology:
During asymptomatic period of about 2 weeks, Bacilli
1. Obstructive causes (50 - 80%)
invade the lymphoid follicles and Peyer's patches of
- Fecolith
small intestine
- Gall stone
↓
- Tumor
Bacilli invade blood stream causing bacteremia
- Ball of worms (oxyuriasis vermicularis)
↓
- Foreign body.
Eventually bacilli are localized in the intestinal
lymphoid tissue, mesenteric lymph nodes, in the liver - Diffuse lymphoid hyperplasia (in children)
gall bladder and in the spleen. 2. Non - obstructive causes:
Note: - Hematogenous spread of generalized infection
- S. typhi are able to survive in gastric acid. - Vascular occlusion
- Once in small intestine, are taken up by and invade - Inappropriate diet lacking roughage.
m-cells. Pathogenesis:
- Organisms are then engulfed by mononuclear cells - Obstruction of lumen →↑ intraluminal
in underlying lymphoid tissue. pressure → stasis, ischemia → Bacterial
proliferation → inflammatory response → V
Morphology
Appendicitis
Gross:
Morphology:
- Site: Terminal ileum commonly
Gross:
- Oval typhoid ulcer with long axis along the
- Normal glistening serosa is converted into dull,
length of the bowel.
granular, red membrane (early acute
- Base of ulcer is black.
appendicitis)
- Margins of ulcer slightly raised.
- Later stage → Abscess formation within wall
- Never significant fibrosis along with ulceration and foci of suppurative
Microscopically: necrosis in mucosa (acute suppurative
- Submucosal peyers patches > 8 cm in diameter. appendicitis)
- Neutrophils accumulate within superficial - Further appendicial compromise leads to large
lamina propria and macrophages containing area of hemorrhagic green ulceration of
bacteria, RBCs and nuclear debris mixed with mucosa and green-black gangrenous necrosis
lymphocytes and Plasma cells in lamina through the wall extending to serosa (Acute
propria. gangrenous appendicitis)
Complications - This stage is followed by rupture and

suppurative peritonitis.
- Perforation of the ulcers and haemorrhage

Pathology
AMOEBIC COLITIS
Etiology
♦ Most common type of amoebic infection caused
by E. histolytica.
Cysts of entamoeba
↓
Ingested through contaminated food and water.
↓
Excystation occurs in small intestine
↓
Trophozoite in colon
↓
Dysentery develops when amoebae attach to
Microscopy: colonic epithelium
- Diagnosis of acute appendicitis requires ↓
neutrophilic infiltration of muscular propria. 1. Lytic action of trophozoites (by cysteine
- Neutrophils and ulceration also present within protease, lectin and amoeba pore)
mucosa. 2. Induce apoptosis, invade crypts and burrow
- Early stage: Congestion and edema of laterally up to lamina propria
appendix wall 3. Recruits neutrophils, causes tissue damage
- Later stage: mucosa sloughed off, wall ↓
necrotic, and blood vessels thrombosed. Creates flask shaped ulcer with a narrow neck
V - Impacted foreign body or fecolith may be seen and broad base.
in lumen. Gross features:
Complication: - Sites: Cecum, Ascending colon, sigmoid colon
- Peritonitis after appendicial perforation. rectum, Appendix.
- Appendicular abscess. - Early lesions appear as small areas of elevation
- Pyelophlebitis with thrombosis of partial on mucosal surface
venous drainage. - Advanced cases → typical flask shaped ulcers.
- Liver abscess. Microscopy:
- Bacteremia - Ulcerated area with chronic inflammatory cells
- Mucocele - Trophozoites of entamoeba in inflammatory
- Adhesion to greater omentum, small intestine exudates and are concentrated at advancing
or other abdominal structures. margin of lesion.
- Edema and vascular congestion in areas
Note: Diagnosis of acute appendicitis may be surrounding ulcers
confused with:
Complications:
1. Mesenteric lymphadenitis. 1. Amoebic liver abscess
2. Sacroilitis 2. Amoebic hepatitis
3. Mittelschmerz 3. Perforation
4. Ectopic pregnancy 4. Hemorrhage
5. Meckel diverticulitis 5. Formation of Amoeboma

GIT
NECROTISING ENTEROCOLITIS ULCERATIVE COLITIS & CROHN'S

♦ Most common in premature infants DISEASE
♦ Incidence of disease inversely proportional to Past Questions:
gestational age. 1. Write gross and microscopic finding in ulcerative
colitis. (1+1=2)[KU 2013]
Pathogenesis
2. Enumerate the important causes of ulceration in
♦ Uncertain large intestine. Describe the gross and
♦ Believed multifactorial in causation. microscopic features of lesions in ulcerative
colitis. (3+3+4=10) [01 June]
♦ In addition to prematurity, most case are
3. Discuss aetiopathogenesis of ulcerative colitis.
associated with enteral feeding. Describe the morphology and complications of
♦ This suggests that some postnatal insult (such as ulcerative colitis. (3+3+4=10) [10 July]
introduction of bacteria) sets in motion, the 4. What is ulcerative colitis? Describe the difference
cascade culminating in tissue destruction. between ulcerative colitis and crohns disease.
(10) [11 July]
♦ No single bacterial pathogen has been linked to
disease Etiology and pathogenesis [10]
♦ Most investigators believe that the two disease
♦ Large no. of inflammatory mediators like platelet
result from a combination of defects in host
activating factor (PAF) has been implicated. interaction with intestinal microbiota, intestinal
♦ These factors promote enterocyte apoptosis and epithelial dysfunction, and aberrant mucosal
compromise inter cellular tight junction immune response.
1. Genetics: NOD -2 Polymorphism
♦ Thus increasing mucosal permeability
2. Mucosal immune responses
♦ This permits transluminal migration of gut 3. Epithelial defects
bacteria leading to vicious cycle of inflammation, 4. Microbiota V
mucosal necrosis and further bacterial entry.
♦ Eventually terminate into sepsis and shock.
Morphology
Gross:
- Site of involvement: Terminal ileum, caecum,
right colon.
- Involved segment is distended, friable and
congested or may be frankly gangrenous.
- Intestinal perforation may be seen.
Microscopy:
- Mucosal or transmural coagulative necrosis
- Ulceration
- Bacterial colonization
- Submucosal gas bubbles.
- Reparative changes like: granulation, fibrosis
Note: Abdominal radiographs often demonstrate gas
within the intestinal wall (pneumatosis intestinalis)

Pathology
Comparing morphology
CROHNS disease Ulcerative colitis [01, 13]
Sites: Terminal ileum, ileocaecal valve, caecum Sites: Rectum, colon
Gross features Gross features
1 Skip lesions 1. Skip lesions are not seen
2. Strictures 2. Pancolitis, ulcerative proctitis, ulcerative
protosigmoiditis or backwash ileitis
3. Apthous ulcer, may progress and multiple lesions 3. Involved colon mucosa is slightly red and granular.
often coalesce into elongated serpentine ulcer along
axis of bowel
4. Cobble stone appearance 4. Broad based ulcers
5. Fissures develop between mucosal folds and may 5. No serpentine ulcers
extend deeply to become fistula tracts
6. Intestinal wall is thickened and rubbery because of 6. Pseudopolyps with mucosal bridges.
transmural edema, inflammation submucosal fibrosis
and hypertrophy or muscularis propria.
7. Creeping fat 7. Mucosal atrophy
8. Serosal surface is normal
9. Strictures do not occur
Microscopy Microscopy
1. Abundant neutrophils infiltration 1. Inflammatory infiltrate
2. Cluster of Neutrophils within a crypt called crypt 2. Crypt abscesses
V abscess
3. Distortion of mucosal architecture 3. Epithelial metaplasia
4. Epithelial metaplasia/pseudopyloric metaplasia 4. Inflammatory process is limited to the mucosa
5. Paneth cell metaplasia 5. Granulomas absent
6. Noncaesating granulomas

GIT
Complications: iv. Loss of SMAD's

v. Loss of p53
Crohns Disease Ulcerative colitis
vi. Activation of telomeres
1. Malabsorption due to 1. Toxic megacolon 2. Microsatellite instability pathway.
impaired fat, B12,
- Multiple mutations occur but of different
protein and electrolyte genes and unlike APC mutation, no
absorption morphologically identifiable changes are seen.
2. Fistula formation 2. Perianal fistula Steps:
i. Basic mutation
3. Stricture formation 3. Carcinoma ii. Loss of DNA repair gene example: TGF-B
4. Malignancy → receptor gene and BAX gene.
lymphoma more often iii. Repetitive DNA sequences (microsatellites)
than adenocarcinoma become unstable during replication cycle
iv. Right sided colon cancer tends to have more
CARCINOMA OF COLON microsatellite instability.
Past Questions: 3. Dietary factors:
1 Discuss the etiopathogenesis of carcinoma colon. Low fiber diet
2. Describe the gross and microscopic features of ↓Stool bulk

carcinoma colon. Add a note on staging of
↑Fecal transit time
carcinoma colon. (3 +2 +2 + 2 + 3 = 10) [04 June]
3. Discuss the etiopathogenesis of carcinoma colon. Stay longer in contact Increased toxic oxidative
Describe the gross and microscopic features of with mucosa byproducts of carbohydrate
carcinoma colon. Add a note on staging of digestion by bacteria V
carcinoma colon. (3 +2 +2 + 2 + 3 = 10) [04 June]
♦ Always comprises of adenocarcinoma Genetic Alteration
♦ Peak incidence 60-79 yrs

Refined diet Potential carcinogen
Risk Factors with low ↑by Normal flora
♦ Excess dietary calorie intake vitamin - A, C, E increased secretion of Bile acids
♦ Low content of unabsorbable vegetable fibers. ↑
♦ High content of refined carbohydrates. High cholesterol intake in red meat
♦ Intake of red meat. Adenoma-carcinoma sequence:
♦ Persistent adenomas Normal colon
Germline/somatic mutation Mutation at APC 5q21
♦ Pre-existing diseases like inflammatory bowel of cancer suppressor genes
disease and diverticular disease.
Mucosa at risk
Pathogenesis [04] Methylation abnormalities Mutation at APC β -catenin
inactiviation of normal alleles
1. APC/β - Catenin pathway.
Adenomas
i. Loss of APC gene (first hit) Homozygous loss of additional Mutation at K-RAS‚ p53
ii. Inactivation of normal alleles (second hit) cancer suppressor genes (Additional mutation)
iii. Point mutation of K-RAS gene Carcinoma

Pathology
Morphology [04] 2. Lymphatic spread

i. Location: 3. Hematogenous spread to liver, lung, brain,
- Ascending colon: 22% bones, ovary
- Transverse colon: 11% Staging

- Descending colon: 6% Based on American joint committee on cancer
- Rectosigmoid colon - 55% TNM classification of colorectal carcinoma
- Other - 6% Tumor
ii. Gross features: Tis : In sites dysplasia or intramucosal carcinoma
Right sided growth T1 : Tumor invades submucosa
- Large cauliflower like, soft, friable mass T2 : Tumor invades into, but not through,
projecting into lumen (fungating, polypoid muscularis propria
carcinoma) T3: Tumor invades through muscularis propria
- Obstruction is uncommon T3a : Invasion < 0.1cm beyond muscularis
- Later, the neoplasm may penetrate the bowel propria
wall and appear as subserosal and serosal T3b: Invasion 0.1cm to 0.5 cm beyond
white firm mass. muscularis propria
Left Sided growth T3c : Invasion > 0.5cm to 1.5cm beyond
- Annular, encircling lesions that produce so msucularis propria
called "Napkin ring" constrictions of the bowel T3d: Invasion > 1.5cm beyond muscularis
- Margins of Napkin ring are heaped up, beaded
V propria
and firm and the mid region is ulcerated. T4: Tumor invades adjacent organs or visceral
- Lumen is markedly narrowed. peritoneum
- Proximal bowel may be distended. T4a : Invasion into other organs or structures.
iii. Microscopy: Similar in both sides T4b : Invasion into visceral peritoneum
- 95% → Adenocarcinoma of varying grades out Regional lymphnodes
of which 10% are mucin secreting colloid Nx : Lymph nodes can't be assessed.
carcinoma.
N0: No regional lymph node metastasis.
- Range from tall columnar cells invading
N1: Metastasis in one to three regional lymph
submucosa, muscularis propria to
nodes.
undifferentiated, frankly anaplastic mass.
N2: Metastasis in four or more regional lymph
- Desmoplastic stromal response
nodes.
- Sometimes mucin with in the cell: Signet ring.
Distant metastasis
Spread
Mx : Distant metastasis can't be assessed
1. Direct spread: most common
M0 : No distant metastasis
- Circumferentially into bowel wall
M1: Distant metastasis or seeding of abdominal
• Directly into depth of bowel wall to serosa,
organs.
pericolic fat, peritoneal cavity

GIT
POLYPS OF LARGE INTESTINE c. Inflammatory polyp (pseudopolyp)

Classification d. Lymphoid polyp
1. Non-neoplastic polyp: 2. Neoplastic polyp:
a. Hyperplastic polyp a. Adenoma (Tubular, villous, tubulovillous)
b. Hamartomatous polyp b. Polypoid carcinoma
- Juvenile polyp: Cystically dilated c. Familial polyposis syndrome:
- Peutz - Jeghers polyp: Tree like branches of - Familial polyposis coli, Gardner's syndrome,
muscularis mucosa [MCQs 013 KU] Turcot's syndrome, Juvenile polyposis
syndrome
Comparison of tubular and villous adenoma
Tubular adenoma Villous adenoma
- Most common (75%) Neoplastic polyps - Less common than tubular
- Mean age of occurrence: 3rd decade - In 6th decade of life.
- Usually Asymptomatic - Usually symptomatic
- Site: most often in distal colon and rectum - Distal colon and rectum.
Grossly:
- Single or multiple - Round to oval exophytic masses
- Sessile or pedunculated - Usually sessile
- Size vary from < 1cm to large spherical masses with - Size vary from 1 - 10 cm diameter
an irregular surface
- Usually, the larger lesions have recognizable stalks
Microscopy: V
- Branching tubules embedded in lamina propria - Presence of many slender, finger like villi which
- Lining epithelial cells are of large intestinal type with appear to arise directly from area of muscularis
diminished mucus secreting capacity, large nuclei mucosa
and increased mitotic activity. - Each papilla has fibrovascular stromal core that is
covered by epithelial cells.
Malignant transformation: low risk - High risk

Pathology
Genetic:
ACUTE PANCREATITIS - Mutations in the cationic trypsinogen (PRSS1)
♦ It is reversible pancreatic parenchymal injury, and trypsin inhibitor (spink1) genes
associated with inflammation. Mechanical
♦ In acute pancreatitis, glands can return to normal - Gallstones
if underlying cause of pancreatitis is removed. - Trauma
♦ In contrast, chronic pancreatitis is defined by - Iatrogenic injury
irreversible loss of exocrine pancreatic
- Operative injury
parenchyma.
- Endoscopic procedures with dye injection
Etiopathogenesis Vascular
Etiologic factors - Shock
Metabolic: - Atheroembolism
- Alcoholism - Vasculitis
- Hyperlipoproteinemia Infections
- Hypercalcemia - Mumps
- Drugs (e.g. azathioprine)
Pathogenesis:

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GIT

biological, physical and antigentic properties of reabsorption.

Clinical features: b. Heat stable enterotoxin

FAST TRACK BASIC SCIENCE MBBS -75-

4. Factors involved in resistance to acidic pH: Enteric fever (05)

2. Culture: d. Bile culture: To detect chronic carrier in whom

FAST TRACK BASIC SCIENCE MBBS -79-

-80- FAST TRACK BASIC SCIENCE MBBS

FAST TRACK BASIC SCIENCE MBBS -81-

Clinical features of cholera (08) iii. Microscopy:

-82- FAST TRACK BASIC SCIENCE MBBS

b. Biochemical tests: i. Campylobacter media (37° for 3-5 days)

FAST TRACK BASIC SCIENCE MBBS -83-

Clinical syndrome: d. Antigen detection:

-84- FAST TRACK BASIC SCIENCE MBBS

2. Pseudo membranous colitis: VIRAL DIARRHOEA

FAST TRACK BASIC SCIENCE MBBS -85-

↓ ♦ The fibre is the organ of attachment and is a

Note: No inflammation occur and the diarrhoea is ♦ Transmission: By fecal oral

Laboratory diagnosis (10,11) Pathogenicity

a. Stool collected in dry container, emulsified in - Incubation period: 24 - 48 hrs

-86- FAST TRACK BASIC SCIENCE MBBS

PARASITES (GIT PARASITOLOGY) - Parabasal bodies: Two curved median bodies

FAST TRACK BASIC SCIENCE MBBS -87-

Life cycle: • Indefinite abdominal pain, nausea, vomiting

↓ a. Ag-detection: By ELISA, fluorescent method

-88- FAST TRACK BASIC SCIENCE MBBS

Entamoeba histolytica (04,05) - Contain small dot like structure, central in

-90- FAST TRACK BASIC SCIENCE MBBS

Life cycle (10) Pathogenesis of amoebiasis (10)

FAST TRACK BASIC SCIENCE MBBS -91-

a. Intestinal amoebiasis: 2. Diagnosis in Asymptomatic carrier (Cyst passer)

-92- FAST TRACK BASIC SCIENCE MBBS

Complication of E. Histolytica infection - Anterior end: Thin, has mouth surrounded by 3

II. Unfertilized eggs: Pathogencity (10)

hypersensitivity reaction such as fever,

Laboratory diagnosis (08, 10) Male worm:

ii. Intermediate host: Not required. B. Symptoms due to adult worms

b. General examination of stool: Necator Americanus

2. Filariform larvae: Infective stage Clinical manifestation

-98- FAST TRACK BASIC SCIENCE MBBS

b. Concentration method: In case flight infection Egg:

FAST TRACK BASIC SCIENCE MBBS -99-

Pathogenecity: • Gravid uterus: Consist of longitudinal

-100- FAST TRACK BASIC SCIENCE MBBS

ii. Ocular type: B. Human cysticercosis

FAST TRACK BASIC SCIENCE MBBS -101-

Diphylobothrium latum II. Procercoid larva

-102- FAST TRACK BASIC SCIENCE MBBS

• Nausea, vomiting, diarrhea - Size: 50-60µ× 30µ

FAST TRACK BASIC SCIENCE MBBS -103-

- Infection can be transmitted due to ♦ Habitat:

- Nocturnal enuresis - It lives in intestine for many years.

- Inflammation of the vermiform appendix may Male worm:

- Pelvic or perineal granulosus rarely occurs. Female worm:

- As they are seldom excreted in faeces, stool - Size: 50µ × 25µ

Egg released in faeces, complete development occurs Laboratory diagnosis

FAST TRACK BASIC SCIENCE MBBS -105-

Bacterial Food Poisoning

- Meat, milk and - Abdominal cramps

-106- FAST TRACK BASIC SCIENCE MBBS

Mycotic Poisoning • Amanita Virosa

FAST TRACK BASIC SCIENCE MBBS -107-

SPECIAL POINTS FOR MCQs