Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

3rd path test > Pathology of the respiratory system (Castleman) > Flashcards

Pathology of the respiratory system (Castleman) Flashcards

1
Q

Bronchi

anatomy

A
  • Have cartilage and glands in their walls
    1. cartilage maintains patency; prevents collapse
    2. Thick connective tissue prevents infection spread into surrounding alveolar parenchyma
    3. Chronic inflammation results in dilation
    4. Changes in diameter increases resistance markedly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Bronchi

Cytodynamics of Epithelial repair

A
  • Cytodynamics of Epithelial repair
    1. ciliated cells are terminally differentiated
    2. epithelial regenerative capacity
      • mucous cells
      • basal cells
      • other nonciliated cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Bronchiole

anatomy

A
  • No cartilage or glands in walls
    1. airway patentcy maintained by tethering support of interalveolar septa on bronchiolar wall
    2. Thin connective tissue in wall allows infection spread to surrounding alveoli
    3. Chronic inflammation results in stenosis of lumen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Broncioles

cytodynamics of Epithelial repair

A
  1. Ciliated cells are terminally differentiated
  2. Epithelial regenerative capacity
    • Mucous cells
    • Nonciliated (Clara cells)
      • Rich in cytochrome monooxygenase enzymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pulmonary lobue

A
  • Primary lobule (Acinus)
    • pulmonary tissue supplied by terminal bronchiole
    • supplied by terminal brionchiole
  • Secondary lobule
    • composed of many primary lobules
    • constitute grossly visible lobules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Interalveolar septa

A
  • Epithelial cells
    • type 1
    • type 2
      • surfactant
      • stem cells
  • Capillary endothelium
  • Fibroblasts
    • elastin
    • collagen
  • Macrophages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Type 1 epithelial cells

A
  • Large surface area
  • susceptible to damage
  • incapable of division
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Type 2 epithelial cells

A
  • cuboidal
  • produces surfactant
  • produces other mediators
  • effect epithelial repair
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which of the followig is not a stem cell for epithelial repair in bronchi and/or bronchioles (which cells are terminally differentiated)?

  • A. Mucous cells
  • B. Ciliated Cells
  • C. Nonciliated cells
A
  • B. Ciliated cells are terminally differentiated and can’t divide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which of the following serve as stem cells for epithelial repair in the interalveolar spetum?

  • A. Type 1 alveolar epithelial cells
  • B. Type 2 alveolar epithelial cell
  • C. Mucous cell
A
  • B. Type 2 alveolar epithelial cells

*With pulmonary carcinoma it’s the type 2 cells that usually divide uncontrollably

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Bronchitis and Bronchiolitis

A
  • Definition
    • Inflammation of bronchi and bronchioles
  • Causes
    • infectious
      • viral
      • bacterial
      • fungal
      • parasitic
    • Toxic
      • 4-ipomeanol and other plant toxins
    • Hypersensitivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Bronchitis and Bronchiolitis

Functional Consequences

A
  1. Increases airway resistance
    • airway obstruction
      • airway wall thickening, accumulation of exudate
    • hypoxemia
      • ventilation/perfusion abnormalities
  2. Decrease mucociliary clearance
    • predispose to secondary bacterial infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Bronchitis and Bronchiolitis

Sequelae

A
  1. Resolution and epithelial repair
  2. Extension to alveoli
    • Pneumonia
  3. Chronic localized inflammation
    • Bronchi: Bronchiectasis
    • Bronchioles: Bronchiolitis obliterans
  4. Post-obstructive atelectasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Bronciectasis

Definition

Pathogenesis

A
  • Definition
    • Dilation of bronchi behond normal physiological limits due to destruction of the bronchial wall
  • Pathogenesis
    1. Chronic infection
      • usually bacterial
    2. Neutrophil-mediated tissue destruction
      • destruction of glands and cartilage
      • fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Bronchiectasis

Morphology: Gross

A
  1. Dilated of airway
    • Saccular or cylindrical
  2. Thick wall
  3. Luminal exudate
    • Grey, green or tan thick mucoid or caseous
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Bronchiectasis

Functional Significance

A
  1. Increase airway resistance
    • Due to turbulence and luminal obstruction
  2. Poor mucociliary clearance
  3. Aspiration of infective material to alveoli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Bronchiectasis

Sequelae

A
  1. Bronchiectasis is irreversible
  2. Progression of inflammation
    • Continued bronchial damage
    • Pneumonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Bronchiolitis Obliterans

Definition

A
  • Obstruction of the bronchiolar lumen by fibrous connective tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Atelectasis

Definition

A
  • Collapse of the lung

*Normal lunch should be pink because it’s got a lot of air in it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Atelectasis

Classification

A
  1. Neonatal
    • inadequate surfactant
  2. Acquired
    • compressive
    • obstructive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Atelectasis

Compressive

A
  • Fluid, air, mass compresses lung or results in loss of negative pleural pressure
  • Animals with well developed secondary lobules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Atelectasis

Pathophysiologic significance

A
  • Segment of lung is underventilated
  • Hypoxemia
    • if widespread
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Atelectasis

Sequelae

A
  1. Resolution of cause: Reinflation
  2. Alveolar edema
  3. Seondary bacterial pneumonia
  4. Fibrosis and irreversible collapse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Pulmonary Emphysema

Definition

A

Enlarged gas-filled space in lung

  • Classification:
    1. Alveolar emphysema
    2. Interstitial emphysema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Collateral ventilation

A

equilization of pressure across lungs due to interalveolar pores (little defect in alveolar walls)

*animals with well developed secondary lobules are isolated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Alveolar Emphysema

Pathophysiologic Significance

A
  1. Decrease alveolar and capillary surface area
  2. Loss of radial support for airways: early closure
  3. Decrease elastic properties; increase compliance and residual lung capacity
  4. Loss of capillary area
    • pulmonary hypertension and cor pulmonale
      • leads to inc load on R. side of heart

*Alveolar emphysema is irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Interstitial Emphysema

Definition

A
  • Excess gas in the pulmonary interstitial
    • occurs in species with extensive interlobular septa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Interstitial Emphysema

Pathogenesis

A
  1. Forced expiration against obstructed airways
  2. Gas dissects into interstitial tissue
    • Interlobular septa
    • Perivascular areas
    • Subpleural tissues

*Cattle with thoracic skin emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Interstitial Emphysema

Pathophysiologic significance

A

Compression of lobules decreases ventilation

-restrictive lung disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Interstitial Emphysema

Sequelae

A
  1. Resolution
  2. Progression
    • mediastinum and subcutis
  3. Secondary infection of pockets
  4. Fibrosis and parenchymal loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Pulmonary edema

Causes

A
  • Inc hydrostatic pressure
    • associated with cardiac dz
  • Inc vascular permeability
  • Hypoalbuminemia
  • Obstruction of lymphatics
  • Inc Na
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

The most common cause of bronchiectasis is?

  • A. Viral infection
  • B. Chronic dust inhalation
  • C. Chronic bacterial infection
A
  • C. Chronic bacterial infection => neutraphils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Which of the following is reversible?

  • A. Bronchiectasis
  • B. Bronchiolitis obliterans
  • C. Atelectasis
  • D. Alveolar emphysema
A
  • C. Atelectasis
    • plural effusion
34
Q

Pneumonia

Simple morphologic classification

A
  1. Bronchopneumonia
  2. Interstitial pneumonia
  3. Focal or multifocal pneumonia
    • embolic
  4. Mixed pattern
    • id: bronchointerstitial
  • Modifiers
    • Duration: acute, subacute, chronic
    • Distribution: focal, multifocal, locally-extensive, diffuse
    • Exudate: necrotizing, fibrinopurulent, granulomatous
35
Q

Bronchopneumonia (95%) vs Interstitial pneumonia (5%)

36
Q

Bronchopneumonia

Pathogenesis

A
  1. Initial deposition of causative agent in terminal bronchioles and alveoli
    • often bacteria, foreign material
      • aspiration
  2. Early damage is in proximal acinar areas with spread into surrounding alveolar parenchyma
37
Q

Bronchopneumonia

Mrophology: Gross and microscopic

A
  • Gross
    1. cranioventral
    2. may be intercurrent fibrinous pleuritis
      • common in horses, cows, and sheep
      • this may be what elicits most dramatic clinical signs
    3. may spread to have lobar distribution
    4. chronicity: fibrosis and lymphadenomegally
      • ​​fibrosis as pleural adhesions
  • Microscopic
    1. Abudant exudate in alveoli including
      • neutrophils
      • fibrin
      • necrotic debris (edema fluid)
    2. Lesions initially airway oriented
38
Q

Bronchopneumonia

Pathophysiologic significance

A
  1. Obstructive and restrictive pathophysiologic changes
    • airway obstructed
    • infiltration of walls and filling of alveoli => makes lungs stiffer
    • exudate and alveolar wall thickening creastes diffuse barrier
      • decreased diffuse capacity
  2. Pleuritis may contribute to restrictive dz
    • decrease in tidal volume
39
Q

Bronchopneumonia

Sequelae

A
  1. Resolution
  2. Death
  3. Septicemia
  4. Chronic bronchopneumonia with bronchiolitis obliterals and bronchiectasis
    • +/- plueral adhesions
40
Q

Interstitial pneumonia

Pathogenesis

A
  1. Primary injury to elements of the interalveolar septum
    • epithelial
    • endothelial
  2. Causes
    • infectious
    • toxic
    • hypersensitivity
  3. Infectious agents
    • virus
    • protozoa
    • some fungi
    • rarely bacterial
      • eg: associated with bacteremia
41
Q

Interstitial penumonia

Morphology: Gross and microscopic

A
  • Gross
    • Often diffuse or locally extensive, firm, large, red, with muscle or liver consistency on cut surface
  • Microscopic
    • Early type 1 epithelial necrosis
    • Subacute: type 2 epithelial hyperplasia, alveolar septal thickening, mononuclear cells
    • Chronicity marked by fibrosis
42
Q

Interstitial Pneumonia

Pathophysiologic significance

A
  1. Thickening and infiltration of alveolar walls marked by increased stiffness and decreased compliance
    • restrictive dz
  2. Decreased diffusion capacity
    • hypoxemia
43
Q

Interstitial pneumonia

Sequelae

A
  1. Resolution
  2. Death
  3. Fibrosis of interalveolar septa and progressive restrictive lung disease
44
Q

Pneumonia

Simple morphologic classification

A
  1. Bronchopneumonia
  2. Interstitial pneumonia
  3. Focal or multifocal pneumonia (embolic)
  4. Mixed pattern
    • bronchointerstitial
  • Modifiers
    • Duration: acute, subacute, chronic
    • Distribution: focal, multifocal, locally-extensive, diffuse
    • Exudate: necrotizing, fibrinopurulent, granulomatous, etc
45
Q

If the distribution of pneumonia is cranioventral, the most likely morphologic diagnosis would be:

  • A. aspiration pneumonia
  • B. fungal pneumonia
  • C. viral pneumonia
  • D. bronchopneumonia
  • E. Interstitial pneumonia
A
  • D. Bronchopneumonia
46
Q

If it is bronchopneumonia, the most likely cause(s) is/are:

  • A. Bacteria
  • B. Virus
  • C. Aspiration
  • D. A and B
  • E. A and C
A
  • E. Bacteria and aspiration

*viruses do predispose the animal to secondary bacterial infections

47
Q

If the pneumonia is diffuse, the least likely cause is:

  • A. Virus
  • B. Protozoa
  • C. Toxins
  • D. Aspiration
  • E. Bacterial septicemia
A
  • D. Aspiration
48
Q

Acute Viral Pneumonia

Pathogenic Essentials

A
  1. Viruses replicate in respiratory airway and alveolar epithelial cells
  2. Virus induces inflammatory and immune response
  3. Inflammation in parenchyma is focused on interalveolar septa
  4. Viral replication is effectively halted before diffuse interstitial pneumonia develops
49
Q

Acute Viral pneumonia

Morphologic features

A
  1. Virus-induced epithelial injury and inflammation
    • Rhinitis
    • Tracheitis/Bronchitis
    • Bronchiolitis
    • Patchy interstitial pneumonia
      • spread contained by effective antiviral response

*Pattern of ‘c and d’ = bronchointerstitial pneumonia

  • garbage can term….lol
50
Q

Canine Adenovirus 2 infection

A
  • Very effective vaccine exists
  • Initially replicated in upper respiratory tract
    • trachea
    • bronchi
  • When it goes into lung it hits bronchioles
    • bronchiolitis
    • replicates in airway eipthelium: non-ciliated cells and mucous cells
  • Progression
    • patchy interstitial pneumonia (replicates in type 2 alveolar epithelial cells)
      • more damage around airways, less damage deeper in lung
    • 5-6 days after inoculation immune response stops replication
  • Lesions tend to be cranioventral
51
Q

Chronic Viral Pneumonia

Pathogenic Essentials

A
  1. Often associated with viruses that replicate in macrophages and/or depress or escape antiviral immunologic defense mechanisms
  2. Virus spreads throghout the lung and induces diffuse interstitial pneumonia
  3. Examples:
    • Lentiviruses (retroviruses)
      • escape immune defenses
    • Immunosuppressive examples
      • Ovine progressive pneumonia
      • Canine distemper virus
52
Q

Bacterial Pneumonia

Patogenic essentials

(pneumonic pasteurellosis: mannheimia (Pasteurella) haemolytica

A
  1. Colonization of respiratory tract
  2. Depression of pulmonary defense mechanisms
    • viruses
    • stress
    • dehydration
    • particulates (crowding, indoors)
  3. Exponential growth of mannheimia haemolytica with leukotoxin production
  4. Damage to neutrophils, macrophages, release of endotoxin
  5. Leukotoxin and endotoxin-mediated tissue damage
    • accentuated by neutrophil release of toxic molecules
53
Q

Bacterial Pneumonia

Acute Lesions

A
  • Bronchopneumonia
  • Diffuse fibrinous pleuritis
    • manheimia
    • pasteurellas
    • mycoplasmas
54
Q

Bacterial pneumonia

chronic lesions

A
  • Widespread fibrosis of pleura (white)
    • restrictive pleuritis
  • Nodular appearance possible from secondary infection
    • pasturella multocida
    • truperella pyogenes
55
Q

Acute respiratory viral infections often induce pulmonary lesions including

  • A. Bronchitis
  • B. Bronchiolitis
  • C. Patchy interstitial pneumonia
  • D. Diffuse interstitial pneumonia
  • E. A, B, and C

*influenza, parainfluenza, adenovirus

A
  • E. Brochitis and Bronchiolitis (kennel cough), and patchy interstitial pneumonia

*

56
Q

What mechanism accounts for some respiratory viruses being able to induce chronic pneumonia and diffuse interstitial pneumonia?

  • A. They replicate in type 1 epithelial cells
  • B. They replicate in type 2 epithelial cells
  • C. They evade or suppress immunological defense mechanisms
A
  • C. They evade or suppress immunological defense mechanisms

* Because it is diffuse they have to evade defense mechanisms

*Respiratory viruses being able to induce pneumonia is because of B . They replicate in type 2 epithelial cells

57
Q

Bovine Toxic Interstitial Pneumonia

Pathogenetic Essentials (5)

A
  1. Ingestion of pneumotoxin
    • L-tryptophane/3-methylindole
    • moldy sweet otatoes (4-ipomeanol)
    • Perilla mint (purple mint)
    • stinkwood (ziera arborescens)
  2. Ruminal conversion and/or intestinal absorption
  3. Activation of pneumotoxin by pulmonary cytochrome P450 monooxygenase
  4. Covalent binding or free radical damage by metabolites and pulmonary cell death
  5. Pulmonary cells most susceptible to toxic injury
    • nonciliated bronchiolar cells
    • type 1 alveolar epithelial cells
    • capillary endothelial cells
58
Q

Think of toxic interstitial pneumonia if….

A
  • cattle/horses that die and lungs show patterns of
    • interstitial pneumonia
    • bronchial necrosis
    • no inflammatory/immune response
59
Q

Toxic Interstitial Pneumonia

A
  • Type 1 epithelial cells
    • large surface area
    • susceptible to damage
    • incapable of division
  • If Diffuse proliferation of Type 2 cells, indicates a interstitial pneumonia
  • Diffusesness might mean hematogenous spread
60
Q

Which of the following pulmonary injuries is most likely to induce the most severe irreversible lung and pleural damage?

  • A. Viral infection
  • B. Bacterial infection
  • C. Dietary pneumotoxins
A
  • B. Bacterial
    • lots of neutraphils
    • lots of fibrin that is corrected by fibrosis then adhesions
      • persistent restrictive mechanism
61
Q

Which of the following contain toxins activated by pulmonary cytochrome P450 monoxygenase to induce interstitial pneumonia in cattle and/or horses?

  • A. Moldy sweet potatoes
  • B. Mold damaged corn
  • C. Purple mint (Perilla mint)
  • D. A, B, and C
  • E. A and C
A
  • E. A and C Moldy sweet potatoes and Purple mint
62
Q

Pulmonary Neoplasia

age of onset

Classification

A
  • More common in dogs and cats than other spp
    • dogs: 10-11 yo; cats: 12-13 yo
  • Common simple classification
    • benign epithelial tumors
      • Adenoma
      • Papilloma
    • malignant epithelial tumors
      • Adenocarcinoma
      • Carcinoma
      • Squamous cell carcinoma
      • Adenosquamous carcinoma
      • Bronchial gland carcinoma
    • sarcoma (fibro, osteo…)

*metastatic neoplasia is the most common form of neoplasia in the lung

63
Q

Pulmonary Neoplasia

Gross Distribution

Biological behavior of carcinomas

A
  • Gross distribution: most common in caudal lungs
    • any lobe can be affected
  • Biological behavior of carcinomas
    • metastasize locally:
      • thorax
      • lung
      • lymph node
    • distant metastasis:
      • lymph node
      • kidney
      • liver
      • spleen
      • bone
      • brain
      • nail bed in cats
64
Q

Histologic features of carcinomas

A
  • obliteration of normal architecture
    • replacement by papillary or acinar-like infiltrates of cells with high nuclear:cytoplasmic ratio
65
Q

The most common form of pulmonary neoplasia is

  • A. Adenoma
  • B. Adenocarcinoma
  • C. Fibrosarcoma
  • D. Leiomyoma
  • E. Metastatic
A
  • E. Metastatic
66
Q

Viral pneumonias in dogs

A
  1. Canine Distemper
  2. Canine Influenza
  3. Canine Adenovirus type 2
  4. Parainfluenza type 2 virus
  5. Canine respiratory coronavirus
  6. Canine herpesvirus 1
    • more imp to younger dogs

*All will induce a patchy, interstitial pneumonia

*kennel cough CS

67
Q

Canine distemper

Pathogenesis

A
  • Respiratory/oropharyngeal inoculation
  • Replication in oropharyngeal lymphoid tissue and viremia
  • Replication in lymphocytes, epithelial cells, monocytes/macrophages cell lineages, nervous tissue cells
  • Failure of cell/humoral/natural immunity leads to penetration of the blood-brain barrier and severe encephalomyelitis

*pancytopenic

68
Q

Canine distemper

Respiratory lesions

A
  • Rhinitis, pharyngitis, tracheitis, bronchitis, bronchiolitis
  • Patchy to diffuse interstitial pneumonia or bronchointerstitial pneumonia
    • may appear as bronchopneumonia if secondary bacterial infection
  • Cytopathic effects
    • intranuclear and intracytoplasmic inclusions in epithelial cells and macrophages (cytoplasmic inclusions predominate)
    • syncytial cells
69
Q

Canine Distemper

Non-Respiratory lesions

A
  • Gastrointestinal (diarrhea)
  • Lymphoid (lymph nodes, spleen, thymus)
  • Dermatitis, Conjunctivitis
  • Cystitis, other urinary tract lesions
  • Teeth: enamel hypoplasia
  • Nervous tissue; Eyes
70
Q

Canine Distemper

A
  • Diagnosis at Necropsy
    • Submit tissue for histopath
      • lung
      • brain
      • thymus
      • lymph node
      • spleen
      • stomach
      • urinary bladder
    • PCR (tissues/swabs)
      • respiratory panel PCR on swabs
        • distemper
        • coronavirus
        • CAV2
        • Parainfluenza
        • H3N8/H3N2; H1N1
        • Canine herpesvirus 1
        • Bordetella bronchiseptica
71
Q

Canine Influenza Virus

Virus isolates

A
  • H2N8 recognized in 2004 in Florida
  • H3N2 emerged in 2007 in South Korea; 2015 in Chicago
    • produces more severe clinical dz
  • Both produce similar dz
72
Q

Canine flu

Disease

A
  • Most commonly seen in shelters, kennels, dog day care, etc
  • H3N8 first seen in racing greyhound dogs
  • Highly contagious
  • Fever and persistent coughing in dogs
    • +/- nasal d/c
    • +/- pneumonia
    • fatality (10%)
      • often seen with secondary pneumonia
73
Q

Canine flu postmortem

Respiratory and histo lesions

A
  • Lymphocytic or suppurative rhinitis
  • Erosive/hyperplastic tracheitis, bronchitis and bronchiolitis
  • Tracheal/bronchial gland epithelial cell necrosis/hyperplasia with lymphocytes/neutraphils
  • Patchy interstitial pneumonia (bronchointerstitial pneumonia)
  • Suppurative bronchopneumonia with secondary bacterial pneumonia
    • mild to severe
74
Q

Morph dx

A
  • Bronchopneumonia
    • cranioventral
    • firm
    • red
  • Probs culture out bacteria
75
Q

Emerging viral respiratory agents

A
  1. Canine pneumovirus
    • similar to PVM in rodents
  2. Canine bocavirus
    • parvoviridae related to minute virus of canines
76
Q

Mycotic Pneumonias in dogs

A
  1. Blastomycosis
  2. Histoplasmosis
  3. Coccidioidomycosis
  4. Pneumocystosis
  5. Cryptococcosis
77
Q

Blastomyces dermatitidis

(Didn’t have time to cover in lecture)

A
  1. Granulomatous pneumonia and pyogranulomatous pneumonia
    • mycelial and yeast forms in lesions
    • yeast forms: 5-25 micrometer diameter
    • doubly refractile, broad-based budding
    • stains: PAS and GMS
78
Q

Blastomyces dermatitidis

Lesions

(didn’t have time to cover in class)

A
  1. Extrapulmonary lesions
    • skin, liver, spleen, lymph nodes, kidneys, eyes
  2. Lung lesions confused with disseminated carcinomas
    • blastomycosis in young dogs: 2-5 yo
79
Q

Coccidioides immitis

(didn’t have time to cover in class)

A
  1. Granulomatous pneumonia and pyogranulomatous pneumonia
  2. Spherules: 20-100 micrometer diameter with endospores
  3. Ruptured spherules: induce neutrophil infiltrates
    • pyogranulomous lesions
  4. Extrapulmonary lesions
    • lymph nodes
    • spleen
    • bone
80
Q

Pneumocystis carinii

(didn’t have time to cover in class)

A
  1. Diffuse interstitial pneumonia
    • unusual manifestation for fungal dz
  2. Associated with immunosuppresion
  3. Ribosomal RNA sequence: fungal
    • most consistent with fungal (controversial)
  4. “trophozoites” (1-4 micrometers) attach to type 1 cells, induce damage
  5. Cysts (5-7 micrometers) in alveolar spaces
    • are detectable by GMS and PAS
81
Q

Cryptococcus neoformans

(didn’t have time to cover in class)

A
  1. More commonly induces encephalitis and nasal/sinus infections
  2. Pneumonia common if immunosuppression
  3. Induces granulomatous pneumonia
  4. Organisms 1-7 micrometers diameter with 1-30 micrometer diameter capsule
    • PAS, GMS positive

3rd path test (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions