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Glossary of Microbiology 12

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enteroviruses -- resistant to low pH (3)?
YES
how do you differentiate rhinoviruses from enteroviruses?
Rhino grow at lower temps than the enteroviruses

Rhino cannot pass the stomach acidity

cause common cold and occasionally respiratory disease in children
Polioviruses
narrow host range; relatively resistant to inactivation; anterior motor neurons --> flaccid paralysis
distribution of poliovirus lesions in the brain
in the cerebral cortex restricted to the precentral gyrus; those in the cerebellum to the roof nuclei; widespread in the brain-stem centers
entry / spread of poliovirus
enters via mouth, spread in mouth & intestine; persists in feces; then moves to Peyer's patches in ileum --> deep cervical and mesenteric nodes (lymphatic stage); then viremic phase --> neurological phase
Salk vaccine
for polio, a trivalent formalized or killed virus vaccine
Sabin vaccine
for polio, a trivalent live attenuated virus vaccine
post polio syndrome
individuals with a history of poliomyelitis develop health problems characterized by fatigue, muscle pain, joint pain, muscle weakness, cold intolerance, atrophy; fxnal problems
Group A coxsackieviruses
extensive myositis and flaccid paralysis
Group B coxsackieviruses
focal muscle lesions, fat pad necrosis, liver, heart pancreas, etc; spastic paralysis
name seven clinical syndromes associated with coxsackie A viruses
(1) herpangina

(2) aspectic meningitis

(3) paralytic disease

(4) febrile exanthems macular: vesicular

(5) lymphonodular pharyngitis (fever and enanthem)

(6) infantile diarrhea

(7) minor illness (including common-cold)
name eight clinical syndromes associated with coxsackie B viruses
(1) pleurodynia

(2) aseptic meningitis

(3) paralytic disease (uncommon)

(4) myocarditis in neonates

(5) pericarditis

(6) respiratory disease

(7) febrile exanthems

(8) minor illness
ECHOviruses
Enteric Cytopathogenic Human Orphan
name six clinical syndromes associated with ECHO viruses
(1) aseptic meningitis

(2) encephalitis, ataxia or paralytic disease

(3) febrile exanthems

(4) respiratory disease

(5) diarrhea

(6) minor illness
are sensory neurons affected in polio?
NO
what is the leading cause of death from NI
nosocomial pneumonia
what is the most important risk factor for nosocomial pneumonia?
endotracheal intubation
nosocomial pneumonia: early onset causes
Strep pneumoniae, H. influenza, Moraxella catarrhalis
nosocomial pneumonia: late onset causes
gram negative aerobes, E. coli, Klebiella, Pseudomonas
nosocomial pneumonia: early or late onset causes
anaerobes, Legionella, respiratory viruses
prions
small proteinaceous infectious particles which resist inactivation by procedures that modify nucleic acids
Kuru (tremors)
fatal debilitating disease found only in the Fore tribe in New Guinea; ingested brain tissue of dead relatives for religious reasons
JCD
characterized by loss of motor control, dementia, paralysis, wasting, and eventually death, typically following pneumonia
FFI
Fatal Familial Insomnia

non-inflammatory lesions, vacuoles, amyloid protein deposits and astrogliosis

sever selective atrophy of the thalamus
Alpers syndrome
prion disease in infants
scrapie
fatal encephalopathy of sheep; incubation period of 4 months to 5 years
BSE
Bovine Spongiform Encephalopathy ("Mad Cow")
SSPE
Subacute Sclerosing Panencephalitis (SSPE)

rare complication of measles virus infection and develops 1-10 years after the initial infection
PML
Progressive Multifocal Leukoencephalopathy

rare, progressive, fatal, demyelinating disease of the CNS which kills oligodendrocytes; results in memory loss, loss of co-ordination, entasia problems (spasms), vision problems, etc

caused by certain members of the papovavirus family, usually JC virus
PRP
Progressive Rubella Panencephalitis

very rare consequence of rubella virus infection, results in mental and motor deterioration

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Bronchopneumonia

Gross: Note multiple, focal (perilobular), yellowish areas of pneumonic consolidation filled with purulent exudate. At autopsy, edema fluid could be expressed from the less affected intervening areas.

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Bronchopneumonia

Low power: Pink, homogeneous, intraalveolar edema; hemorrhage and fibrin; a blue area in a bronchus composed of neutrophils.

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Bronchopneumonia

High power: The blue area under high power. The bronchus is filled with desquamated epithelial cells, debris and neutrophils (pus). This is an example of purulent bronchiolitis which impairs aeration of distal alveoli until exudation is expectorated.

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Bronchopneumonia

First stage of pneumonia: Edema. High power: Pulmonary edema. Congestion of arterioles and capillaries. Desquamated alveolar lining the cells in alveoli. Neutrophils are scanty.

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Bronchopneumonia

Second stage of pneumonia: Red hepatization. This stage is referred to as red hepatization in lobar pneumonia because the consolidated lobe of the lung has the consistency of liver. The alveoli contain red cells and fibrin.

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Bronchopneumonia

Third stage of pneumonia: Gray hepatization. Low power: Alveoli are filled with fibrin and neutrophils. The congestion of vessels is receding.

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Bronchopneumonia

Fourth stage of pneumonia: Area of lysis. Shows disintegrated neutrophils, some edema and a predominance of macrophages. Proteolytic enzymes have lysed the fibrin. Neutrophils are seen in alveolar walls and macrophages have removed the cellular debris.

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Bronchopneumonia

High power: macrophages.

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Lobar pneumonia

Gross: Note the diffuse pneumonic infiltration of the entire middle lobe (gray hepatization stage) with fibrinous exudate involving the pleura and interlobar fissures.

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Lobar pneumonia

Low power microscopic: The alveoli show a uniform infiltration of neutrophils. The pleura shows anthracosis and chronic fibrosis perhaps related to a previous episode of pneumonia. Note that all alveoli show the same stage of pneumonic infiltration and compare this with bronchopneumonia.

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Bacterial endocarditis

Gross view: Mitral valve opened to show row of vegetations on the margins of cusps.

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Bacterial endocarditis

A view of vegetations on a valve cusp. Note how friable they appear. They have a tendency to break off and produce "septic" emboli which in turn produce "septic" infarcts in various organs.

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Bacterial endocarditis

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Gross: Acute cholecystitis.

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Acute cholecystitis

Lower power : Note ulceration of surface mucosa. The underlying wall is edematous and hemorrhagic. The inflammatory reaction is transmural, leading to separation of muscle layers and a serosal exudate. This can progress to perforation and peritonitis.

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Gross: Appendicitis.

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Normal appendix: Note the appearance and relationship of mucosa, lymphoid follicle, muscularis and serosa.

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Acute appendicitis: Observe necrosis of the mucosa. At this magnification the diffuse neutrophilic infiltration of the muscularis is just recognizable.

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Acute appendicitis

Detail of ulcerated necrotic mucosa infiltrated by purulent exudate.

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Gross: Acute bacillary dysentery showing diffuse ulceration of mucosa. The greenish-yellow foci are remnants of partially necrotic mucosa. The mucosa may finally reepithelialize with regeneration of the normal villous pattern. Since the damage is limited to the mucosa, this disease does not result in stricture.

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Bacillary dysentery

Lower power: Small bowel. The glands have almost disappeared and only the basal portions can be recognized. The mucosa is now composed of necrotic tissue covered with a fibrinous pseudomembrane. A true membrane overlies normal tissue. A pseudomembrane consists of necrotic tissue which after removal leaves an ulcerated surface.

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Bacillary dysentery

High power: Pseudomembrane.

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Gross: Tuberculosis of testis and epididymis.

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Lower power: Tuberculosis of epididymis with the portion of ductus deferens in the center.

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TB Testis & Epidydimis

Higher power: For orientation, the slide has a portion of ductus deferens in one corner, venous plexus in the second corner and a dark blue lesion with a central necrotic core separated from the surrounding tissue in the third corner. Between these three structures is a round, pink lesion surrounded by a blue rim of lymphocytes. This is a proliferative tubercle.

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TB of Testis / Epidydimis

Higher power: This section shows a duct and a giant cell tubercle; a round nodule with a large Langhans giant cell in the center surrounded by fibroblasts; and occasional lymphocytes.

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Caseous TB of lung

Gross view of areas of caseous necrosis.

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Lab 1.8 Caseous TB of lung

Edge of necrotic area with giant cells.

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Caseous TB of lung

In this slide a stain for "acid fast" bacilli has been used (Ziehl Neelson method). A little search in the areas of caseous necrosis will reveal clusters of bright red rods which represent tubercle bacilli.

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Miliary TB of lung

When a caseous focus ruptures into a blood vessel, rapid vascular spread of infected material occurs. Consequent "seeding" may take place and a large number of tubercles of roughly the same age and size are formed. These are the so-called "miliary" tuberculosis (millet sized granuloma). This can occur in the lungs, liver, spleen, bone marrow, kidney, etc. An important feature is little or no caseation in the granulomas.

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Fibrocaseous TB of lung

Lower power: Note large area of caseation surrounded by fibrous tissue.

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Fibrocaseous TB of lung

High power: Shows edema and lymphocytic infiltration.

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Fibrocaseous TB of Lung

Langhans giant cell surrounded by epithelioid cells and early fibrosis. During its natural course, the lesions of pulmonary tuberculosis show a marked variation in the tendency to heal or progress. Most favorably the lesions might fibrose and calcify, but still contain viable bacilli. Less favorably, the caseous foci could spread via air passages (tuberculous bronchopneumonia), or lymphatic and blood vessels (miliary tuberculosis). Caseous erosion of a bronchus leads to coughing up of the necrotic material and formation of a cavity. Erosion of blood vessels causes blood-staining of sputum or massive hemoptysis.

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Granuloma (Histoplasmosis)

Gross: Lung with walled-off, calcified lesions. On X-ray--coin lesions.

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Granuloma (Histoplasmosis)

A walled off granuloma showing a marked similarity to tuberculosis. The specific diagnosis of histoplasmosis would depend on identification of the organisms or more indirectly on a positive serological test.

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Varicella

Low power: Epidermis with intraepidermal blisters. The superficial layer is intact. The cystic spaces are in the prickle cell layer.

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Varicella

Higher power: A cyst filled with edema fluid. At the base there is a viral inclusion body.

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Varicella

High power: Intranuclear inclusion bodies.

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Cytomegalovirus of lung and kidney

Higher power: Several large cells one of which is dark pink and contains a viral inclusion body.

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Cytomegalovirus of lung and kidney

Neonatal kidney showing viral inclusion bodies filling the cell nuclei.

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Molluscum Contagiosum

This viral disease produces 1-2 mm pinhead-sized skin lesions with a central depression. This slide shows the complete lesion of proliferated squamous epithelium filled with eosinophilic inclusion bodies. These are the largest known inclusion bodies, thus they are visible on low power scanning.

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Molluscum Contagiosum

Higher power: Molluscum lesion

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Syphilis of Aorta

Destruction of medial elastica leads to mural weakening and aneurysmal dilatation. The aneurysm can rupture, or compress and erode adjacent structures. The aortic cusps may be rolled and the commissaries may widen, which can cause aortic valve incompetence.

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Syphilis of Aorta

The "tree barking" effect produced in the intima by the medial scarring.

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Syphilis of Aorta

Higher power: Perivascular "cuffing."

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Syphilis of Aorta

Normal aorta elastic stain.

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Syphilis of Aorta

Disruption and destruction of elastic tissue in aortitis.

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Candidiasis of Kidney

Low power: Nearly half of this field shows an area of parenchymal necrosis and leukocytic infiltration - an abscess - within which radiating mycelia are seen.

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Candidiasis of Kidney
Higher power: A glomerulus is occupied by fungus. Hyphae are indiscriminately growing through normal tissue boundaries. Note the lack of tissue reaction which indicates the patient's diminished response to the organism.

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Candidiasis of Kidney

Fungi are seen in the adjacent abscess area.

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Candidiasis of Kidney

High power: Shows branching of hyphae.

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Chromoblastomycosis of Skin

Severe hyperplasia of skin. Eosinophilic keratin overlying thickened prickle cell layer with elongated papillae. There is diffuse dermal inflammatory infiltration and a micro abscess in one papilla.

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Chromoblastomycosis of Skin

High power: Note two intraepithelial abscesses and a subepithelial granuloma containing giant cells. (High power microscopic examination may show thick walled fungi in the abscesses).

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Chromoblastomycosis of Skin

Note the brown fungus in the center of the abscess.

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Blastomycosis of Lung

Shows diffuse infiltration of lung with abscess resembling confluent pneumonia.

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Blastomycosis of Lung

Higher power: Shows histiocytic and a giant cell granuloma. Note one of the giant cells contains a fungus with double contoured cell wall.

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Blastomycosis of Lung

The nuclear structure of this fungus can be seen in the thick wall organisms.

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Coccidioidomycosis of Lung

Low power: Shows large areas of necrosis.

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Coccidioidomycosis of Lung

Shows two mature sporangia, one of which has just ruptured. Note the neutrophilic reaction.

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Coccidioidomycosis of Lung

Immature sporangia. The clear halo is the cell wall. These fungi are often engulfed by giant cells.

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Cryptococcosis of Lung

Note the bluish staining fungus surrounded by the red mucin stained capsule. The budding of the fungus is clearly seen. This organism produces granulomata and abscesses in the lungs and other organs particularly the meninges.

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Toxoplasmosis of Brain

Brain shows infarct/necrosis. Toxoplasma gondii is a parasite that frequently does not cause tissue damage. Disease results from massive infection or immunodeficiency. Fetal intrauterine infection (particularly of brain) can occur.

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Toxoplasmosis of Brain

Toxoplasma cyst containing toxoplasma organisms.

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Toxoplasmosis of Brain

Individual toxoplasma organisms lying free in brain tissue.

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Amebic Colitis

Shows the typical undermining ulcer of amebic colitis.

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Amebic Colitis

Base of ulcer. Note absence of inflammatory response. Amoeba are in necrotic membrane above the muscle coat.

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Amebic Colitis

Note amebae in mucosal glands. Erythrocytes can frequently be seen in Entamoeba histolytica.

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Amebic Colitis

Numerous amebae are present.

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Pneumocystis Carinii (H&E)

Low power: The alveolar spaces almost universally contain pink proteinaceous exudate.

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Pneumocystis Carinii (H&E)

Medium power: In most instances the pink exudate does not quite fill the alveoli, and in some places vacuoles or irregular spaces are seen. This gives the exudate a characteristic "foamy" or "cloudy" appearance.

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Pulmonary Aspergillosis

Aspergillus species may infect abnormal airways (e.g. old tuberculous of bronchiectatic cavities) and remain non-invasive. In immunocompromised patients, however, this fungus may invade the lung parenchyma, causing a severe, often necrotizing, pneumonia. In this section, taken from the lung of an organ transplant patient, the bronchial lumen is virtually filled by a mass of fungal hyphae.

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Pulmonary Aspergillosis

Higher power: Note the hyphae invading the bronchial wall.

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