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general pathology > Morphologic Diagnosis 2 > Flashcards

Morphologic Diagnosis 2 Flashcards

1
Q

What are the 7 steps in microbial disease?

A
  1. ) Access body through a port of entry
  2. ) Contact target cell (tissue/organ)
  3. ) Colonize & amplify in target cell (tissue/organ)
  4. ) Spread locally, neighboring cells (tissues/organs)
  5. ) Spread systemically (blood, lymph, PNS)
  6. ) Colonize LN and/or distant tissues
  7. ) Injure or kill [distant] target cells (tissues/organs)
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2
Q

What are the possible cell outcomes / mechanisms of injury?

A
  • Directed cellular disfunction
  • Malignant transformation
  • Structural injury
  • Cell death (necrosis)
  • Persistent / latent infection
  • Cellular proliferation
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3
Q

Will inflammation occur with any of the possible cell outcomes?

A

Inflammation may occur along with many cell outcomes.

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4
Q

What is the scientific name of Pisttacosis?

A

Chlamydophila (Chlamydia) psittaci

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5
Q

What kind of bacteria is Chlamydophila (Chlamydia) psittaci? How does it survive?

A
  • Gram (-) bacterium
  • Obligate intracellular (depends on the host’s ATP)
    Needs hosts ATP to proliferate.
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6
Q

What is the mechanisms of injury for psittacosis?

A

Mechanisms of injury:

  • Cell death (necrosis)
  • Persistent or latent infection
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7
Q

What is the pathogenesis of psittacosis?

A

Elementary Bodies enter cells via endocytosis or phagocytosis

  • They Blocks fusion of endo/phagosome + lysosome (so it can replicate)
  • Elementary Bodies turn into Reticular Bodies ( in order to reproduce)
  • Reticular bodies replicate by binary fission
  • Reticular Bodies turn back into Elementary Bodies to leave the cell.
  • Elementary Bodies leave cell:
  • Via Lysis or exocytosis
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8
Q

What is the purpose of elementary bodies? Reticular bodies?

A

Elementary bodies are more hardy, can be used to infect or leave cells. They cannot reproduce though, that is only done by the reticular bodies.

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9
Q

Why is psittacosis significant? What Birds are known to be the highest infected?

A
  • Zoonotic disease
  • May be fatal in immunocompromised
  • Pigeons are highest reported, followed by raptors.
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10
Q

What is the transmission route of psittacosis? What is important about the bacteria in the environment. What kind of disease can it cause in humans?

A

Transmission:
- Via respiratory droplets, feather dust,
feces
- Inhalation, ingestion or mucosal
(conjunctival) contact
-Survives desiccation
In humans Respiratory disease may be severe, even if you are not immunocompromised you can get bad pneumonia.

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11
Q

What is a way that psittacosis can be aerosolized?

A
  • If someone is sweeping infected feces it can aerosolize infection and cause pneumonia.
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12
Q

What is occuring in this histological image of a bird liver? What is the condition associated with it?

A

Psittacosis - Necrosis ( coagulative necrosis -> still has some cell shape/ sinus outlines)

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13
Q

What is another name for psittacosis?

A

Pirates disease

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14
Q

What is the morphologic diagnosis of this gross image? What condition has gross morphology like this?

A

Acute, severe, multifocal necrotizing hepatitis.

You can also say -> acute diffuse severe fibronous pericarditis.

Psittacosis

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15
Q

What is the morphologic diagnosis of this histological slide? What is a likely etiologic diagnosis?

A

Acute severe heterophilic necrotizing multifocal hepatitis

Etiological diagnosis: Bacterial hepatitis

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16
Q

What is being indicated by the yellow arrows? The blue arrow?

A

Yellow arrow: macrophages with unicellular debris.

Blue arrow: Dead heterophils

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17
Q

What is one way to diagnose Psittacosis? What is the most ideal way to diagnose it?

A

You can do a gram stain to see if it is a gram negative bacteria. Since you cant differentiate it from another gram negative bacteria you should use, machiavelli stain, since the elementary bodies will apear a periwinkle color. To be 100% sure you must use IHC or In situ hybridization.

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18
Q

What stain is depicted here for this gram negative bacteria? What is the bacteria and what can be seen in this image?

A

Machiavelli stain - you will see elementary bodies staining a periwinkle color. This is psittacosis.

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19
Q

What is the brown around this cell indicating? What kind of stain is this? What is it usually used in?

A

This is IHC. The brown is the target which shows your histology is positive. This is positive for psittacosis.

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20
Q

What birds are affected by avian pox?

A

Any bird species can be affected by Avian pox.

> 200 bird species are susceptible

  • Some species specificity
  • Domestic fowl & canaries particularly susceptible
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21
Q

What kind of virus is avian pox?

A

Genus Avipoxvirus of the Poxviridae
- DS DNA enveloped

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22
Q

What is this stain and what is it highlighting? What in this stain is the bright pink areas?

A

This is a gram stain, and the bright pink ares are showing the gram negative bacteria in this sample of tissue.

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23
Q

What is the route of transmission for avian pox?

A

Transmission:
- Insect bites, skin lacerations

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24
Q

What forms of avian pox are there? What is most common?

A
  • Dry and wet form
  • Dry form typically affects area of skin that is less feathered or unfeathered.
  • Wet form affects the pharynx and esophagus. Causes diptheric membrane in trachea/ esophagus

Dry form is the most common

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25
Q

What is the condition seen in this image?

A

Dry Avian Pox

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26
Q

What is diptheric membranes?

A

They are the term used to describe necrosis of the lumen of a tubular organ.

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27
Q

What can be seen in this image?

A

The characteristic dumbell shape of pox virus on Electron microscopy

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28
Q

What kind of electron microscopy must be used to see avian pox?

A

Transmission.

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29
Q

What are the mechanisms of cellular injust in avian pox?

A

Mechanisms of cellular injury:

  • Cell death (necrosis)
  • Directed cellular disfunction
  • Persistent or latent infection
  • Cell proliferation
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30
Q

What is the pathogenesis of avian pox?

A
  • Virus enters target cell ( usually epithelium)
  • Replications in cytoplasmvia cell mechanism
  • Viral gene encodes epidermal growth factor causing HYPERPLASIA
  • Large Inclusion bodies formed (Bollinger bodies)
  • Virus release via Budding OR cell necrosis (most likely)
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31
Q

What is more hardy, an enveloped or non eneveloped virus?

A

Non enveloped virus

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32
Q

What is directed cell dysfunction?

A
  • virus takesover cell and has it make proteins for its capsid.
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33
Q

What is the number one mechanism of cellular injury for avian pox?

A

Cell proliferation (REMEMBER HYPERPLASIA)

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34
Q

What is seen in this image? What is the cause?

A
  • Mechanical damage can cause hemorrhage/ ulceration. This is from avian pox (dry) (cutaneous form)
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35
Q

What is another potential issue with cutaneous (dry) avian pox?

A

They are susceptible to secondary bacterial infection.

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36
Q

What are characteristics of normal avian skin?

A
  • Normal avian skin (thin)
  • Keratinized
  • Basement membrane -> 3-4 layers of epidermal skin -> and stratum corneum
37
Q

Is this epidermal sample abnormal?

A

No it is normal bird skin

38
Q

What is seen in this histologic slide of avian skin?

A

Thickened skin with large cells. Cells are not empty, pink things inside cells are inclusion bodies. This is typical presentation of pox virus. Not another virus will typically give you this presentation.

39
Q

What is occuring in this image? What are the yellow arrows pointing at? The black arrows?

A

Pink areas pushing nucleus aside are inclusion bodies, this is typical apperence of avian pox.

Yellow arrows -> individual large cells

Black arrows -> Inclusion bodies -> millions of them.

40
Q

What is the name of the inclusion bodies of avian pox?

A

bollinger bodies

41
Q

What is the morphologic diagnosis of these images?

Etiologic diagnosis?

Disease name?

A

Morphologic diagnosis: Acute severe diffuse necrotizing/ proliferative dermatitis

42
Q

What are teleost fish?

A

Non cartilaginous fish

43
Q

What are the main signs of lymphocystis?

A
  • Cytomegaly - cell enlargement
  • Karyomegaly -> nucleus enlargement
44
Q

What is seen in this image? What kind of elecronmicroscopy is used to obtain this view?

A

In the blue you can see the typical viral hexagonal appearence)

  • Tranmission EM
45
Q

What is lymphocystis? Who does it affect? What kind of virus is it?

A
  • Non cartilaginous fish
  • DNA virus
  • Iridoviridae
  • Non-enveloped
46
Q

What is the main mechanisms of cell injury in lymphocystis?

A
  • Directed cellular disfunction
  • Cell proliferation
47
Q

What is the target cell for lymphocystis?

A

Fibroblasts

48
Q

What is the routes of transmission for lymphocystis? Where are lesions usually located? What kind of fish species are affected? Is this disease malignant?

A

Route of transmission: ¡ Ingestion, direct contact, ‘inhalation’

Location: Skin & gills, but also internal organs

Affects Many teleost fish species
Has Low mortality (benign disease) unless affects the individual to a point they cant see or eat, swim, ect.

49
Q

What is seen in this image? What is the large dark puple area in the upper left corner? What are the small dots surrounding the large cell?

A

This is a fibroblast with lymphocystis. It is up to a million times larger than normal. The fibroblast keeps growing and growing.

The small dots are the nuclei of normal sized cells. The large dark purple area is the nucleus of the infected cell.

50
Q

What is a concern for lymphocystis that can change the prognosis?

A

The presence of secondary bacterial infections.

51
Q

What occurs to the cells in lymphicystis? What kind of inflammation is present?

A

Non suppurative inflammation, lymphoplasmacytic

Eventual cell death, can infect adjacent cells.

Has macrophage/ lymphocyte inflammation.

52
Q

What can occur in lymphocystis if the fish does not die from complications associated from the lesion?

A

It will either remain the same or eventually regress.

53
Q

What is the morphologic diagnosis for this histologic slide? Etiologic diagnosis?

A

Chronic Focal with karyomegaly, basophilic cytoplasmic inclusions and moderate lymphoplasmacytic dermatitis

Etiologic diagnosis:

Viral Dermatitis

54
Q

What are the 3 types of prion TSE’s focused on? Which is zoonotic?

A

Transmissible Spongiform Encephalopathies:

  • Bovine Spongiform Encephalitis – zoonotic (vCJD)
  • Scrapie (sheep & goats)
  • Chronic Wasting Disease (deer & elk)

Scrapie and CWD not known to be zoonotic.

55
Q

What is seen in this histological slide? What does it look like? What can this cause ?

A
  • Vacuoles being produced within neurons ( vacuolation ) due to prions.
  • Looks like a sponge.
  • Makes the animal continously lose weight and become emaciated, if you do not euthanize the animal will die from this emaciation.
56
Q

What is the mechanism of cell injury for TSE?

A
  • Progressive degeneration nervous system
  • Directed cellular disfunction
  • Structural injury
  • Persistent or latent infection
57
Q

What is indicated by the purple lines, and what is indicated by the blue lines in this histological slide?

A

Purple is vacuolated neurons

blue is normal neurons,

58
Q

How can you obtain prions? What is the pathogenesis of TSEs?

A
  • ingestion is method of transmission ( maybe inhalation/ mucosal contact)
  • M cells in intestines are where prion particle begins infection. It is picked up by dendritic cells/ macrophages. -> It replicates in lymphoid tissues -> spreads to other lymph nodes -> Systemic spread -> gets to brain ( mechanism unclear, thought is via leukocyte trafficing or could be retrograde) -> once in brain creates these CNS lesions.
59
Q

How do prions cause metabolic dysfunction of neurons/ neural cells?

A
  • Conversion of normal Prpc to PrPSc
  • Accumulation of protease-resistant β-sheet isoform of PrPSc

in short -> changes normal protein to prion protien/ mutated protein.

60
Q

What are the steps of change from normal protein to prion protein?

A

Explaination corresponds to the image attached with numbers indicating the steps.

1.) Prion protein looks similar but is slightly different. Slightly different in a way that makes the protein useless. “ kinda similar, but kinda useless”

2 .) and 3.) Prion interaction begins to cause normal protein to change shape and replicate as the useless prion protein.

3.) This useless protein begins to accumulate in the cytoplasm. You cannot get rid of it.

Essentially a buld up of alot of useless protein and loss of function of normal protein.

61
Q

Why is the accumulation of prions so problematic?

A

No one knows exactly why it is such a big deal. It is alot of accumulated prion protein “ not goof to have alot of junk in your cytoplasm” and a loss of the needed proteins.

62
Q

Are prions alive? Can they survive in the environment?

A

Prions are not alive, they can be in the environment since they aer not alive and just sit there.

63
Q

Where is it difficult to import from due to concerns for BSE?

A

Alberta Canada.

64
Q

What species can get chronic wasting disease? Is this a wild animal problem?

A

White tailed Deer, Mule Deer and Moose.

Can be found in captive and domestic species.

65
Q

What does the brain look like grossly in patients with CWD? What about Histologically?

A

Grossly brain looks normally so you must look histologically. You will have the spongiform areas of vacuolated neurons within the brain. You must do IHC to be sure targeting the prion protein.

66
Q

What is occuring in this image? What condition is it? What is the red areas? What wis the yellow arrow pointing at?

A

This is a slide indicating CWD, the red areas are IHC stain targeting prion protien, showing the presence of prion proteins in red. The yellow arrow is showing the vacuole.

67
Q

TRUE or FALSE:The vacuole itself in TSE neural tissue contain prion protein.

A

FALSE

It does not contain the prion protein.

68
Q

TRUE or FALSE: You can look for TSE on a brian that has been sitting around

A

FALSE

You must have fresh brain tissue. Any decay/ autolysis will cause vacuoles so you will not be able to tell if it is a spongiform disease or if it is just a normal post mortem change.

69
Q

What is the morphologic diagnosis for TSE? Etiological Diagnosis? Is there any inflammation?

A

Chronic moderate diffuse, neuronal vacuolation, spongiform, with degeneration, and necrosis encephalitis

No there is not any inflammation

Etiologic Diagnosis: Prion spongiform Encephalitis

Name of disease: Transmissible Encephalitis

70
Q

With scrapie, what can be seen even before you begin to see signs of emaciation?

A

Before seeing emaciation you can see signs of paresthesia, due to abnormal sensation of skin without apparent casue.

71
Q

What is paraesthesia?

A

Paresthesia: abnormal sensation of the
skin (tingling, pricking, chilling, burning, numbness) with no apparent physical cause.

72
Q

What animals are at risk of transmissable veneral tumors? What kind of disease is this? What is its route of transmission.

A

Strays/ dogs allowed to roam, mostly in southern US/ Mexico. Not very common in north america.

Route of transmission: Sexual transmission

STD.

73
Q

What is seen in this histological image?

A

This is showing alot of round cells ( round cell tumor, or TVT)

74
Q

What is notable about the round cells found with TVT?

A

Enlarged nucleus

75
Q

What is the abnormal lone cell this image?

A

Mitotic figure of neoplastic cell. Has abnormal mitosis since it is neoplasia.

76
Q

Is it a pathogen that causes TVT? What is being spread? What kind of cell is it?

A

Tumor cell causes the disease not a pathogens. It is not the dogs own cell that is becomeing neoplastic, they are being infected by a neoplastic cell ( imortal cell) that continues to replicate and create more of itself.

77
Q

What testing can determine if this is TVT vs another kind of cancer cell?

A
  • The dna of tumor will have different DNA than host cell. The tumor also has less chromosomes than the host cell
78
Q

How many chromosomes do the normal host cells have in dogs with TVT? What about in the neoplasia cell? What kind of transfer is occuring with this tumor? What is the likely cell type?

A
  • 59 chromosomes in neoplastic cell. vs 78 in normal dog cells
  • It is transfered via xenograft, and is proably histiocytic.
79
Q

How does canine TVT evade immune destruction? What occurs with the tumor over time?

A
  • These cells make enough MHC-I to avoid being killed by natural killer cells, (self) as well as not enough to be picked up by cytotoxic T cells/ lymphocytes (non self) and make no MHC-II to avoid detection.

Eventually lymphocytes catch up and they produce IL-6 and INF-y and then they start to produce more MHC- I and can be recognized as non self.

Tumors can regress over time, but usually they keep growing and growing, causing severe lesions.

80
Q

What animals are susceptible to TVT? What areas of the body can be infected?

A

Dogs, coyotes, foxes, and wolves

  • Sexual transmission
  • Urogenital / other mucosae (ocular, nasal, oral)
81
Q

What is the likely cause of this lesion?

A

Canine TVT

82
Q

What is indicated by these black arrows?

A

Black arrows are showing more normal mitotic figures,.

83
Q

What is a way they can treat Canine TVT?

A
  • usually surgically
  • Now treating with vincristine.
84
Q

What is likely the cause of this lesion?

A

Canine TVT

85
Q

What is the cause of the lesion seen in this image?

A

Lymphocystis

86
Q

What is the likely cause of the abnormalities in this image? If told this is a 3 year old moose what would be your concern? What about if it was a 1 year old cow? A mink?

A

TSE

  • Caused by prions

Moose: CVD (Chronic wasting disease)

Bovine: BSE ( Bovine Spongiform Encephalitis)

Mink: TME (Transmissible Mink Encephalitis) Mink Spongiform Encephalitis

87
Q

What is the disease humans can get from BSE?

A

vCJD or

Variant Creutzfeldt-Jakob disease (vCJD) is a prion disease that was first described in 1996 in the United Kingdom. There is now strong scientific evidence that the agent responsible for the outbreak of prion disease in cows, bovine spongiform encephalopathy (BSE or ‘mad cow’ disease), is the same agent responsible for the outbreak of vCJD in humans.

88
Q

What is a common name for Bovine Spongiform Encephalitis?

A

Mad Cow disease

89
Q
A

general pathology (18 decks)

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