OSPE-OSCE MICROBIO-PATHOLOGY SLIDES

Designed by Todinho 1

“Almighty God,Grant unto us that, we may flee to the knowledge of thy loving kindness and

tender mercy;That the storms of life may pass over us, and not shake the peace of God that is

within us.”Amen...

OSPE REVISION

GUSTODIO A DE JESUS

At high power are seen the vacuolated, koilocytotic changes in the squamous epithelial cells from human papillomavirus infection. ("Koilocytosis" refers to vacuolization which is perinuclear).

Koilocytes Basement membrane

3 - Cervix, low-grade squamous intraepithelial lesion (flat condyloma) - Low power

Flat condyloma, or human papilloma virus infection, is characterized by the presence of koilocytes, which are squamous cells with enlarged, wrinkled, dark ("raisinoid") nuclei surrounded by a halo. The cells are usually found in the superficial half of the epithelium.

In this cervical biopsy, the dysplastic, disordered cells occupy about 1/3 to 1/2 the thickness of the epithelium, and the basal lamina is intact, so this is cervical intraepithelial neoplasia (CIN) II. Note that the classification of CIN I, II, and III depends on the extent of the thickness of the epithelium affected

by dysplastic changes; CIN III indicates that dysplastic changes involve the entire thickness of the epithelium.

At higher magnification, cervical dysplasia is demonstrated. Note the disorderly development of the cells from the basement membrane upward at the right, compared to normal maturation at the left. At

the right, the full thickness of the epithelium is involved by the disordered, dysplastic process, consistent with a grade of cervical intraepithelial neoplasia (CIN) III.

Normal squamous epithelium In situ and invasive squamous cancer

5 - Cervix, squamous cell carcinoma - Low power At low power, the abrupt transition between the normal squamous epithelium and

the squamous cell carcinoma (in situ and invasive) can be appreciated.

Cytologic features of dysplasia are seen on Pap smear. Some of the cells at the center show increased nuclear/cytoplasmic ratio, with darker and more irregular nuclei than the normal

squamous cells with large amount of cytoplasm and small, pyknotic nuclei.

The cytologic features of invasive squamous cell carcinoma are demonstrated on a Pap smear. Note the cells with hyperchromatic, pleomorphic nuclei and increased nuclear/cytoplasmic ratio. The

background has inflammatory cells.

Normal squamous cell Dysplastic squamous cells, high grade Endocervical cells

1 - Uterine cervical cytology, Papanicolaou stain (Pap smear) - High power

In comparison to the normal cervical squamous cells, the dysplastic cells have increased nuclear:cytoplasmic ratios with enlarged nuclei and coarsely granular chromatin. The presence of endocervical cells indicates that an adequate specimen was obtained.

Mitotic figures

Basement membrane

2 - Cervix, high-grade squamous intraepithelial lesion (CIN III) - Medium Power

Virtually the entire thickness of the cervical epithelium is affected by dysplastic changes. Note the cellular and nuclear pleomorphism, failure of normal and orderly differentiation, hyperchromatic nuclei, and several mitotic figures extending toward the surface. Only the very superficial cells appear to differentiate and flatten.

Although most of the basement membrane is not completely visible in this image, it is intact.

A loss in the uniformity of the cells as well as a loss in their architectural orientation.(DYSPLASIA)

Pap Smear Results

Cervical Ca Morphology:• Raised (acuminatum) or flat (macular).

• Koilocytotic atypia

• Abundant HPV nucleic acids.

• Atypical cells in the basal region (CIN-1) or completely replace normal cells (CIN-3)

• 3 gross types

– Exophytic/Fungating, Ulcerating & Infiltrative.

• 80% Squamous-Ca, 20% other.

• Adeno-carcinoma, Adenosquamous, Clear-cell carcinoma etc.

• 40-50 peak age

Ulcerating Ca Cx:

4 - Cervix, carcinoma - Gross

This pink-tan, friable, fungating lesion on the anterior cervical lip is characteristic of cervical carcinoma.

Fungating Ca Cx

Tubo-ovarian complex Torsioned tubo-ovarian complex

6 - Uterus, fallopian tubes and ovaries, pelvic inflammatory disease with tubo-ovarian complexes - Gross

The inflamed fallopian tubes and ovaries have coalesced to form huge tubo-ovarian complexes in this typical example of pelvic inflammatory disease. The tubo-ovarian complex on the patient's right has undergone torsion, resulting in hemorrhagic infarction.

Infiltration of synovial stroma

by inflammatory cells

Increased vascularity

aggregation of fibrin and

formation of rice bodies

Formationn of villous

outgrowths of the synovium

activation of osteoclasts

and formation of erosions,

cysts and osteoporosis

vascular granulation tissue

(pannus) destroys the

cartilage, bone and bridges

Fibrous adhesions

RA - Pannus:(synovial hyperthrophy with formation of villi)

Hyperplastic Hyperplastic inflammed inflammed synoviumsynovium

Hyperplastic synovium Lymphoid nodule

5 - Synovium, rheumatoid arthritis - Medium power

This is a higher magnification of the previous image. The reactive synovium is clearly evident. The inflammatory cells are organized into a lymphoid nodule. Recall that the primary lesion of rheumatoid arthritis is synovitis.

Rheumatoid Nodule (skin):

Palisading EpitheloidPalisading EpitheloidMacrophagesMacrophages

CentralCentralFibrinoidFibrinoidNecrosisNecrosisMONONUCLEAR CELLS

Here is a rheumatoid nodule. Such nodules are seen in patients with severe rheumatoid arthritis and appear beneath the skin over bony prominences such as the elbow. They can

occasionally appear in visceral organs. There is a central area of fibrinoid necrosis surrounded by pallisading epithelioid macrophages. and other mononuclear cells

Fibrinoid necrosis Epithelioid histiocytes

8 - Rheumatoid nodule - Low power

Rheumatoid nodules consist of a central zone of fibrinoid necrosis surrounded by a prominent rim of epithelioid histiocytes and numerous lymphocytes and plasma cells. Rheumatoid nodules occur in approximately 20% to 25% of patients with definitive or classic rheumatoid arthritis. Nodules generally are associated with severe articular and systemic disease and with high titers of rheumatoid factor

Articular cartilage

11 - Femoral head, degenerative joint disease - Gross

Osteoarthritis of the hip is common. In this typical image, there is marked irregularity and erosion of the articular surface. Very little articular cartilage remains.

Osteophyte

12 - Femoral head, degenerative joint disease - Gross

In more advanced cases, no cartilage remains, and apposing bones rub together, resulting in eburnation of the bone. Eburnated bone is shiny and smooth, grossly. Histologically, it is sclerotic.

Osteoarthritis: Ankylosis• varus deformity of the

knee and collapse of the joint space with destruction of the medial cartilage and the subchondral cortex (open arrowheads).

Osteoarthritis:• Lateral view of the left

knee shows sclerosis with marked osteophyte formation (arrows). The osteophytes are best seen in this view.

OA:• Subchondral

cysts (solid arrowhead)

OA Fingers:Joint narrow space, ostephyte formation, cyts formation, bone sclerosis, deformity, heberden’s (DIP) node, bouchard’s node (PIP) and decrease bone density

heberden’s node

bouchard’s node

OA Hip: 1997, bilateral, joint space narrowing (arrows) at the hips that is worse on the left side

OA Hip: Subchondral sclerosis (solid arrowhead) and cyst (arrow) formation are also

noted on the left side

Malaria

This damn disease mimics everything and anything…

Diagnostic points:-

Red Cells are not enlarged. Rings appear fine and delicate and there

may be several in one cell. Some rings may have two chromatin dots. Presence of marginal or applique forms. It is unusual to see developing forms in

peripheral blood films. Gametocytes have a characteristic

crescent shape appearance. However, they do not usually appear in the blood for the first four weeks of infection.

Maurer's dots may be present

Dx Points:

1. Red cells containing parasites are usually enlarged.

2. Schuffner's dots are frequently present in the red cells as shown above.

3. The mature ring forms tend to be large and coarse.

4. Developing forms are frequently present.

Dx Points:

• Ring forms may have a squarish appearance.

• Band forms are a characteristic of this species.

• Mature schizonts may have a typical daisy head appearance with up to ten merozoites.

• Red cells are not enlarged. • Chromatin dot may be on the inner

surface of the ring.

Dx Points:

• Red cells enlarged.

• Comet forms common (top right)

• Rings large and coarse.

• Schuffner's dots, when present, may be prominent.

• Mature schizonts similar to those of P. malariae but larger and more coarse.

INVESTIGATION:

Thin film – identify speciesThick film – identify parasites

Interpretation (C):

• Mature schizont of Plasmodium Vivax with:

• Enlarged RBCs

• Multiple merozoites (> 12)

• Fine brown

Chronic Bronchitis

smokers lung – Normal Lung

TB MORPHOLOGY:

Note the subpleural granuloma at the right along with the granuloma in the hilar lymph node, typical findings for the Ghon complex of primary tuberculosis.

On closer inspection, caseous (cheesy appearance) tan necrotic tissue is seen to constitute the granulomas in this gross appearance of a Ghon complex. Most patients with primary tuberculosis are asymptomatic, and the granulomas resolve.

Extensive cavitation of multiple granulomas of lung are typical for secondary tuberculosis from reactivation of primary infection or reinfection as an adult. Such lesions have a predilection for appearance in the upper lobes of the lung. Also multiple casseation necrosis

The small millet seed sized granulomas in this lung are typical for miliary tuberculosis.

Note the rounded, focal nature of these granulomas at low power magnification.C

Tubercle Granuloma

Epitheloid cells and T Lymphocytes/larghan giant cells

Note the pink, amorphous region in the center of this granuloma at the upper right, and ringed by epithelioid cells at the left and lower areas of this photomicrograph. This is the microscopic appearance of caseous

necrosis.

Elongated epithelioid cells, which are transformed from macrophages, as well as a Langhans giant cell (a committee of macrophages with the

nuclei arranged at the periphery) are shown here.

Granulomas are not always well-formed, but there should at least be epithelioid cells. Giant cells are often present. Other inflammatory cell components include lymphocytes, plasma cells, and occasional neutrophils. Collagenization

usually indicates a healing response. As granulomas heal, they can become calcified.

An acid fast stain is used to diagnose the presence of mycobacteria in tissue and cytologic preparations. Note the thin red rod-like organisms. What are the steps in this staining

procedure? What color are the white blood cells in this slide? What color are white blood cells in a gram stain? What color are the organisms in this slide? Why? What does "acid-fast"

mean? (AFB: ZIEHL NIELSON STAIN)

More sensitive than an acid fast stain, this auramine stain requires fluorescence microscopy. Note the yellow-orange rod-like

mycobacteria. Of course, the most sensitive method for detection of mycobacteria is microbiologic culture.

Cornea:The avascular cornea is covered anteriorly by a thick stratified squamous epithelium and posteriorly by a cuboidal endothelium lying on Descemet's membrane.

Lens:The lens is covered on the anterior surface by a single layer of cuboidal epithelium. These cells differentiate at the

equator to form lens fibers, which lack distinct organelles, including nuclei. The entire lens is enclosed within a basement membrane, the capsule. Anterior to the lens are sections of the iris.

Ciliary Body:The ciliary body at the base of the iris is responsible for the production of aqueous humor and for the attachment of the zonule ligaments, which attach to the lens and

help control it's degree of curvature.

Ciliary Body:The ciliary body is the site of a transposition of the two layers of epithelium. Notice how

the pigmented layer is below the non-pigmented layer at the green arrow, but the positions have reversed by the blue arrow.

Iris:Within the iris, the more anterior epithelial layer is difficult to distinguish from the heavily

pigmented posterior layer. In fact, the anterior layer has developed into a myo-epithelial layer that serves as the dilator pupillae muscle. The larger muscle at the tip is the contrictor pupillae

muscle.

FoveaIn the absence of overlying optic nerve fibers and other inner retinal layers, the fovea is the area of least refractory distortion and therefore high visual acuity. It corresponds to

the "focus point" in our visual field.

Optic DiscThe retinal ganglion cell axons converge at the optic disc and exit the eye as the optic nerve.

The absence of retinal neurons in this area results in a blind spot.

Histology of retina and optic nerve in glaucoma

Retina

Optic disc, with cupping

Optic nerve

Todi (MBBS3)

The first thing to note in this slide is that, compared with the previous slide (and the following slide), the magnification is different. Nevertheless, the RBC's here are smaller than normal and have an increased zone of central pallor. This is indicative of a hypochromic (less hemoglobin in each RBC) microcytic (smaller size of each RBC) anemia. There is also increased anisocytosis (variation in size) and poikilocytosis (variation in shape).

The most common cause for a hypochromic microcytic anemia is iron deficiency. The most common nutritional deficiency is lack of dietary iron. Thus, iron deficiency anemia is common. Persons most at risk are children and women in reproductive years (from menstrual blood loss and from pregnancy).

This peripheral blood smear demonstrates several ring forms of Malaria (Plasmodium vivax) in the red blood cells.

Here is another example of sickled erythrocytes in a patient with Hgb SS who presented with severe abdominal pain in sickle crisis. The sickled cells are prone to stick together, plugging smaller vessels and leading to decreased blood flow with ischemia.

Monocyte

Segmented PMN

RBCBasophil

Eosinophil

Banded PMN

Platelet

Lymphocyte

A normal mature lymphocyte is seen on the left compared to a segmented PMN on the right. An RBC is seen to be about 2/3 the size of a normal lymphocyte.

The WBC's seen here are "atypical" lymphocytes. They are atypical because they are larger (more cytoplasm) and have nucleoli in their nuclei. The cytoplasm tends to be indented by surrounding RBC's. Such atypical lymphocytes are often associated with infectious mononucleosis.

WBC Morphology DiagramsMorphologic appearances of WBC's on a peripheral blood smear include the findings pictured below. Moving the mouse over each image will reveal the name in the status bar at the bottom.

Left shift

An absolute increase in neutrophils with an increase in bands, and sometimes an increase in immature forms such as metamyelocytes or myelocytes

Hypersegmentation

Polymorphonuclear leukocytes normally have 3 or 4 lobes, but 5 or 6 or more lobes indicate hypersegmentation; seen most often with megaloblastic anemias, sometimes with myeloproliferative disorders, or following chemotherapy (methotrexate)

Toxic granulations Increased number and prominence of the azurophilic (primary) granules; seen most often with bacterial infections and in association with cytoplasmic vacuolization

Döhle body Irregularly shaped blue staining area in the cytoplasm due to free ribosomes or RER; seen with infections

Smudge cell / Basket cell A ruptured cell remnant, classically associated with fragile lymphocytes in CLL

Platelet satellitosis An artefact of EDTA anticoagulation, this may cause the platelet count to be artefactually low

Pelger-Huet anomaly An autosomal dominant condition with neutrophils that are mostly bilobed in the heterozygote (normal function) and unilobate in the homozygote (fatal)

May-Hegglin anomaly Rare disorder with large, prominent Döhle-like bodies

Chediak-Higashi syndrome Rare disorder with large neutrophilic granules representing abnormal lysosomes

Morphologic FindingsThe following terms are used in describing the morphologic variation

seen in WBC's on a standard peripheral blood smear

RBC Morphology DiagramsMorphologic changes seen in RBC's on a peripheral blood smear include the findings pictured below. Moving the mouse over each image will reveal the name in the status bar at the bottom.

Acanthocyte

Cell with irregular, long, asymmetrical projections; sporadically seen with severe liver disease or post-splenectomy; seen with rare disorder of abetalipoproteinemia

Anisocytosis Variation in size of RBC's

Babesiosis Similar to ring forms of malaria

Basophilic stippling Small aggregates of RNA are seen as small blue dots in the RBC; fine stippling may be a feature of reticulocytes; coarse stippling can appear with toxic marrow damage, myelodysplasia, and thalassemias

Elliptocyte Elongated, elliptical cell; non-specific when occasionally seen; rare disorder of hereditary elliptocytosis

Heinz body Precipitated Hgb seen as a perimembranous blue dot only after supravital staining; seen with some hemoglobinopathies

Howell-Jolly body Small, round deeply basophilic nuclear remnant; seen when spleen is absent

Hypochromia Cells with decreased MCH, typical of iron deficiency

Macrocytosis Cells with increased MCV, typical of megaloblastic anemias

Malaria Plasmodium infection seen as "ring forms", stippling, and gametocytes, depending upon the species

Microcytosis Cells with decreased MCV, typical of iron deficiency anemia and thalassemias

Pappenheimer body Multiple, tiny iron containing granular blue dots; seen when spleen is absent and with iron overload

Poikilocytosis Variation in shape of RBC's

Polychromatophilia The bluish tint to young RBC's with high RNA content

Reticulocyte Young RBC's with increased RNA content that can be precipitated by supravital staining for identification and enumeration

Rouleaux Linear aggregation of RBC's that resembles a stack of coins; seen when surface charge is reduced with increased serum protein, particularly increased fibrinogen or globulin

Sideroblast Non-nucleated RBC with stainable iron

Spherocyte Small, round dense cell without central pallor; suggests extravascular (splenic) hemolysis in previously normal persons; with hereditary spherocytosis there is increased osmotic fragility

Schistocyte Fragmented, irregularly shaped seen with intravascular hemolysis such as microangiopathic hemolytic anemias (DIC, TTP). A variant called a "helmet cell" appears cut in half

Sickle cell Curved, banana-shaped cell with pointed ends found in sickle cell disease from aggregation of Hgb S

Stomatocyte Cell with slit-like central pallor; occasional stomatocytes are non-specific or an artefact; many are seen with rare hereditary stomatocytosis

Target cell Cell with central and peripheral staining with intervening pallor due to increased redundancy of RBC membrane; seen with liver disease, in some thalassemias, and with Hgb C

Tear drop cell Cell pinched at one end, prominent in myelofibrosis and myelophthisic conditions

Diabetes Files

“TOGETHER WE WILL MAKE IT HAPPEN”

Normal Pancreatic Islet:

ß cells ß cells (Insulin) αα cells cells (Glucagon)

δδ cells cells (Somatostatin) pp Cells pp Cells (pan prot)

ßß αα

Normal morphology• The islets of Langerhans – 2%

of the mean pancreatic gland – 1-2g

• A cells – glucagon (20%)• B cells – insulin (68%)• D cell – somatostatin (10%)• PP cells – pancreatic

polypeptide (2%)

Pancreatic acini Stromal fat Islets

7 - Pancreas, non-insulin-dependent diabetes mellitus - Low power

This low-power view shows pancreatic acini, stroma with blood vessels, and a few islets of Langerhans. Note that the exocrine part of the pancreas is normal. The changes in the islets are seen better on higher magnification in the next image.

Islet Pancreatic acini Amyloid

8 - Pancreas, non-insulin-dependent diabetes mellitus - High power

In this high-power view, an islet surrounded by normal pancreatic acini is seen. The islet shows extensive deposition of a pink homogeneous material that has the features of amyloid. This

change is often, but not always, seen in long-standing type II diabetes.

An islet of Langerhans demonstrates insulitis with lymphocytic infiltrates in a patient developing type I diabetes mellitus. This lesion precedes clinical onset of diabetes mellitus and is rarely observed.

Islets in Type II Diabetes:Loss of ß cells, replaced by Amyloid deposits (hyalinization)Loss of ß cells, replaced by Amyloid deposits (hyalinization)

An islet of Langerhans demonstrates amorphous pink deposition of amyloid in a patient with type II diabetes mellitus.

Islets in Type II Diabetes:Loss of ß cells, replaced by Amyloid deposits (hyalinization)Loss of ß cells, replaced by Amyloid deposits (hyalinization)

Nephropathy

• Diffuse thickening of the glomerular capillary basement membrane.

• Abnormal mesangium with fibrin casps.

Type II noninsulin-dependent diabetes accounts for the vast majority (90 to 95 percent) of diabetes cases. Unlike the Type I form of the disease, this type of diabetes comes on gradually and is associated with obesity and aging, though there also appears to be a strong genetic component to the condition. The beta cells of Type II diabetics are intact and produce insulin, but the other cells in their bodies have lost the ability to respond to the substance. Since they do not generally suffer form a lack of insulin, however, Type II diabetics do not usually need insulin injections, though they may be utilized in severe cases. Much more commonly, the disease is controlled with diet and exercise.

Renal complications

A renal glomerulus demonstrate nodular glomerulosclerosis with diabetes mellitus. This lesion is quite characteristic for diabetes mellitus. A diffuse glomerulosclerosis may also be seen.

Cont..

The urinary tract can be involved by an ascending urinary tract infection. Diabetics are more prone to develop infections in general. Here are seen budding cells with pseudohyphae with Candida albicans on PAS stain in the renal pelvis.

An acute pyelonephritis. This is the medulla of the kidney showing numerous

neutrophils.

Ascending urinary tract infection

Ocular complications

This is the normal appearance of the retina on funduscopic examination.

Retinopathy• Non Proliferative

– Microaneurysms, – Dot blot hemorrhages– Hard and soft

exudates– Cotton wool – infarcts– Macular edema.

• Proliferative.– Neovascularization – Large hemorrhages– Retinal detachment.

Background retinopathy

Note numerous microaneurisms and some small

dot and blot

haemorrhages

Background retinopathy with many hard exudates

Diabetic retinopathy with hard exudates and oedema

Note that since the exudates and oedema involve the macula, there would be visual impairment

Cotton wool spots or soft exudates (retinal infarcts resulting from arterial occlusion).

haemorrhages

New vessels (neovascularisation) grow into these infarcted areas

Scattered microaneurisms,

blot haemorrhages,

a few hard exudates,

and new vessel formation

Image from Webpath CD

New vessel formation of proliferative retinopathy

This results from new vessel formation, which occurs into the vitreous as well as in the retina. These vitreous vessels rupture, causing a haemorrhage into the vitreous. The patient may complain of “floaters”, as these haemorrhagic bits float free in the vitreous.

A vitreous haemorrhage

Complications of diabetes

• Peripheral cataract • Central cataract

New vessels develop on the anterior surface of the iris in response to severe ocular ischaemia. This results in obstruction of the aqueous drainage and leads to glaucoma. It most commonly occurs in diabetes but may also occur in carotid artery stenosis, retinal detachment, central retinal vein thrombosis, or ocular tumours.

Rubeosis iridis

Diabetic retinopathy is shown here on funduscopic examination. The arrows reveal cotton wool spot (soft exudates), dot hemorrhages, macula, optic disc, multiple yellow lipid exudation, microaneurysm

Cont..

Proliferative diabetic retinopathy on funduscopic examination is shown here. This is a particularly serious complication in diabetics that can lead to blindness.

Label the diagram.

Hard dep.

Optic disc

Macula

Blot hem

Cotton wool

Diabetic Retinopathy

Pre retinal Hemorrhage - detachment

Diabetic foot sepsis, with ischaemia and gangrene

Nephropathy

Cont..

The left anterior descending coronary artery that courses over the anterior surface of the heart shown here is opened to demonstrate a recent red-black thrombus filling the lumen in a patient with diabetes mellitus.

Cont..

The interventricular septum has been sectioned to reveal a large recent myocardial infarction (about 4 to 7 days old) with a tan-yellow necrotic center surrounded by a zone of hyperemia, gross. About half of persons with diabetes mellitus will die from a myocardial infarction as a consequence of coronary atherosclerosis.

Aortic atheroma in a diabetic patient.

Minimal involvement in the aorta at the bottom, severe involvement in the aorta at the top. Diabetics tend to have more advanced extensive atherosclerosis Image and text from Webpath CD

Macrovascular complication

Plaques with ulceration and thrombosis

1 - Aorta, atherosclerosis - Gross, endothelial surface

Involvement of blood vessels, both large and small, is very characteristic of longstanding diabetes. In large blood vessels like the one shown here, there can be severe and extensive atherosclerosis. This change occurs earlier in diabetics than in nondiabetics

Cortical surface Cut surface

3 - Kidney, diabetic nephropathy - Gross

Kidneys are often severely affected in diabetes. This results from vascular disease affecting both the large blood vessels and glomerular capillaries and from increased predisposition to infections. The gross appearance of the kidney varies, depending on the type of vascular lesion. Typically, as seen here, kidneys with diabetic glomerulosclerosis show diffuse, fine granularity of the cortical surface, resulting from destruction and scarring of the glomeruli.

Complications • Microvascular complication leading to a below knee

amputation• Microvascular complication: Amputation of the

digits and a current ulcers

Diabetic Amyotrophy

The diabetic foot

• Ischemic and neuropathic ulceration.

• Traumatic damage in the presence of sensory loss

• Spread infection to bone can cause osteomyelitis

Diabetic gangrene

Vascular disease in diabetes• Macrovascular: disease of the large and

medium sized vessels– not specific to diabetes, but . . . – is accelerated, more extensive in diabetes– includes cardiovascular, peripheral

vascular, cerebrovascular disease

• Microvascular: disease of the small vessels- specific to diabetes- found primarily in the eye, the kidney, the nerves

Microbiology Rs

Interpretation:

• Candida Albicans:• SDAs (Sabouraud Dextrose Agar)

• Whitish, creamish in color

• Eg: vaginitis, oral thrush

• Unable to grow in Blood agar

• In Microscope slide:• Gram positive, budding yeast on culture media, 10x than bacteria size,

filaments if taken directly from infected humans

CLEAR ZONE

NO CLEAR ZONE

ANTIMICROBIAL TEST

Interpretation:

• Antibiotic sensitivity test

• Clear zone- antibiotic is sensitive to bacteria

• No clear zone- bacteria is resistant to antibiotic

1:2 1:4 1:8 1:16 1;32

1:64 1:128 1:2561:512 1:1024

Flocculation

Grey stuff: carbon Ags with cardiolipin

Limitation is:No uniformity- need visualization test

Positive indicates active infectionDilution carries out in 2Higher the dilution, the greater the infection

VDRL test

• Venereal Disease Research Lab: screening test for syphilis because it binds to non-specific Abs (reagin) and only for acute phase

• TPHA/TPPA (Treponema pallidum particle agglutination): specific/confirmatory test for syphilis because it binds to specific Treponema Ags

• Carbon Ags acts as Ab Reagan (non-specific Ab)

• If VDRL positive and TPHA negative: no syphilis

• If VDRL negative and TPHA positive: previous infection or latent infection

• If both positive: active infection

Interpretations:

A: Positive: Mat like (presence of Ag-Ab), agglutination presence, sunny like

B: Negative: Button like/scrambled egg, no agglutinationC: unsensitized (quantitative)D: sensitized (qualitative)- to determine the result of active infection or

not“the higher the dilution, the greater the infection of disease”• Eg; 1:16 means how much load of infection is• Limitation of this test:• 1) not enough sample/blood• 2) subjective (light/dark, eyes)

Mackonkeys Agar (MC):

• Used to distinguish Lactose fermentase (pink) from Non-lactose fermentase (colorless) bacteria

• Most gram –ve bacteria grows but not gram +ve bacteria. Why? Because selective agents (bile salts n crystal violet) will suppress the growth of gram +ve bacteria

• LFs: - non enteropathogenic, pink in media/pigment due to acid produced reacts with PH indicator eg: E.coli, Klebsiella, Enterobacteria

• NLFs: non-pigmented/colorless due no rxn with PH indicator eg: Proteus sp, salmonella, Shigella

Blood Agar (BA)

• To detect hemolytic bacteria esp. streptococcus, staphylococcus, Bacillus, Enterobacteria…

• Used blood• Type of rxns produced:• A. Beta hemolysis: a clear zone around

colonies eg: Streptococcus Pyogens• B. Alpha hemolysis: green discoloration eg:

Streptococcus pneumoniae• C. Gamma hemolysis: colorless

Chocolate Agar (CA)

• For fastidious organisms: Haemoph. Influenza, Neisseria, Enterobacteria, Staphy/Strepto., Bacillus…

• Only for gram –ve bacteria

• Microscopically can be seen: white, opaque, circular, dry colonies

Sabouraud Dextrose Agar (SDA)

• Used to culture Candida Albicans (Yeast) and fungi

NUTRIENT AGAR:•Colorless• uses SDA too if there is yeast/fungi as commensal flora for ears, nose, throat and vagina

OGAWA MEDIA

Made up of eggs and saltsSeen as dry colored light greenShould keep in bottle?•Slow growth (4-6 weeks)•Prevent desiccation•Infectious•Seen as: rough, crumbly, waxy, cream/buff colored

Confirmatory test of TB:•NIACIN TEST•NITRATE REDUCTION TEST

Revision from yr 1 and 2

Central vein

Sinusoids

Renal corpuscle

Mesangium

Glomerular space

Blood vessel

PCT (longitudional)

PCT (Transverse)

Rheumatic fever

Phil 4:12

Acute rheumatic fever - Schematic The inflammatory lesions of acute rheumatic fever affect all three parts of the heart: endocardium (especially valves), myocardium, and epicardium. Endocardial involvement leads to the formation of vegetations (called verrucae) along the line

of closure of the affected valve. The mitral valve is commonly affected, though in many cases multiple valves are involved. Myocardial involvement takes the form of myocarditis with widely disseminated focal inflammatory lesions (called Aschoff bodies) scattered about in the

interstitium, often in a perivascular location. The pericarditis of acute rheumatic fever begins with similar inflammatory lesions of the epicardial connective tissues, and, in many cases, is associated with a fibrinous or serofibrinous exudate. The pericarditis of acute rheumatic fever usually

resolves without lesions, but, in rare cases, it can result in a constrictive pericarditis with dense fibrous adhesions that bind the parietal to the

visceral pericardium.

Morphology:• Acute Rheumatic Fever –

– Acute Inflammatory Phase– Heart – Pancarditis– Skin – Erythema Marginatum– CNS – Sydenham Chorea– Joints/cartillage--Migratory

polyarthritis

• Chronic Rheumatic Fever – Deforming fibrotic valvular

disease.

Acute Rheumatic Fever:

• Aschoff bodies :

• Fibrinoid degeneration

• T lymphocytes

• Anitschkow cells

• Aschoff giant cells

Heart, Aschoff body - High power Inflammatory lesions are found widely scattered in the valves, pericardium, and myocardium of patients who die of acute rheumatic fever (ARF). The cellular aggregate seen above is typical of the myocardial lesions found, and is called an Aschoff body (AB). The typical AB contains plump histiocytes (Aschoff cells), some of which are multinucleated (Aschoff giant cells). The predominance of histiocytic cells, some epithelioid, suggests that the AB is a form of granuloma. Aschoff bodies may also contain lymphocytes and plasma cells. A central zone of fibrinoid necrosis is seen in Aschoff bodies in early stages of ARF. Widespread fibrinoid necrosis and inflammation of the valve substance leads to damage of the overlying endothelial cells. With endothelial damage, thrombosis is initiated, and vegetations form along the closing edge of the valve where the leaflets slam together. This endocardial damage heals with dense fibrous scars, which progress over

time to look like the valves in the images that follow.

The fibrotic thickening of the valve leaflets can also be seen in this view of a mitral valve from a patient with postrheumatic mitral stenosis. This image also shows fusion and thickening of the

chordae tendineae.

5 - Heart, rheumatic mitral valve, chordae changes - Gross

6 - Heart, rheumatic heart disease, rheumatic aortic stenosis - Gross

This valve depicts postrheumatic aortic stenosis. The severe cuspal thickening and fusion of the commissures have distorted the three cusps of the valve so that they appear as a single fused unit, fixed in an open but stenotic configuration. This valve would generate a complex murmur with components of both aortic stenosis

(AS) and aortic insufficiency (AI).

7 - Heart, rheumatic mitral and aortic stenosis - Gross, longitudinal section, cut surface

Both the mitral and the aortic valves are affected. Severe, long-standing, aortic stenosis has resulted in left ventricular hypertrophy. The severe left atrial dilation is a result of mitral stenosis.

Hemosiderin-macrophages

Chronic left heart failure of many different etiologies is often associated with elevated left atrial pressure and elevated pulmonary venous and pulmonary capillary pressure. With mitral stenosis, left atrial pressures can be particularly high. When alveolar capillary pressure exceeds plasma oncotic pressure, fluid leaks out into the alveoli, and the patient develops pulmonary edema. With severe chronic pulmonary congestion, there can also be intermittent alveolar hemorrhage. These hemosiderin-laden macrophages are the residue of prior alveolar hemorrhage; they represent microscopic evidence of chronic severe left heart failure

9 - Heart, bacterial endocarditis - Very low power

This is a mitral valve vegetation in bacterial endocarditis. There are destructive vegetations on both sides of the valve and an abscess-like process is burrowing into the myocardium. The bacteria are visible as a dark blue zone on the surface of the vegetations.

LYMPHOCYTES

FIRBRINOID NECROSIS

MULTINUCLEAR GIANT CELLS

PLUMP MACROPHAGES

ASCHOFF BODIES

A- DILATED BLOOD VESSELSB- HEMOSIDERIN WITH LOADED MACROPHAGES SEEN AS BROWN COLOR

Aschoff’s nodesAschoff’s nodes are the characteristic and pathognomonic granulomatous lesion of rheumatic heart disease.

Giant cells

Histiocytes,

lymphocytes

Fibrinoid necrosis

Rheumatic endocarditis

Normal

Fibrinoid and inflammation

Fibrosis

Calcification and deformation

Rheumatic endocarditisThe damage to the valves heals by progressive fibrosis, with thickening of the valve leaflets and associatid chordae tendineae.

Rheumatic Valve Disease:

• Gross: – Leaflet thickening– Commissural fusion– Shortening, Thickening & fusion of chordae

tendinae.• Microscopic:

– Fibrosis – neovascularisation– Calcification

• Mitral 68%, Mitral+Aortic 25%, • 99% of Mitral stenosis is due to RHD.

Mitral stenosisThickness of the alveolar walls.

Haemosiderin in the lumen of the alveoli.

The cusps of the valve are obscured by the presence of large irregular and friable masses of thrombi, also called vegetations. The vegetations, or thrombi, form due to an underlying damage to the valvular endocardium (endocarditis). Tricuspid endocarditis is typically caused by

organisms (bacteria, fungi) that gain access to the venous circulation, most commonly in intravenous drug abusers via use of nonsterile needles. The microorganisms reach the right atrium and lodge on the tricuspid valve, causing inflammation (endocardial injury), thus providing

an altered endocardial surface on which thrombosis occurs. Such thrombi, or vegetations, are obviously infected.

In some chronically ill patients (eg, those with cancer), there is hypercoagulability of the blood. In such patients, fibrin deposition and consequent vegetation formation occur on normal valves. These

vegetations do not contain bacteria or other microorganisms, and, hence, they do not destroy the valve. Note that the valve retains its normal shiny, smooth surface and is not distorted. However, the

risk of systemic embolism and its consequences remains

Erythema Marginatum:

“It's not that I'm so smart, it's just that I stay with problems longer”--Albert Einstein

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