MEET THE DEFENDERS
A pathogen reaches the respiratory tract but becomes trapped in a sticky secretion and is moved outward by hair-like projections. Name the two innate defenses working together.
Answer: What are mucus and cilia/mucociliary flow?
Explanation: Mucus acts as a physical barrier by trapping pathogens, while cilia provide a mechanical defense by moving mucus and trapped organisms out of the respiratory tract.
A dog has an increased total WBC count caused primarily by an increased absolute neutrophil concentration. Give the proper terms for both abnormalities.
Answer: What are leukocytosis and neutrophilia?
Explanation: Leukocytosis refers to an increased total WBC concentration, while neutrophilia specifically describes an increased neutrophil concentration. The slides emphasize comparing absolute concentrations with the reference interval.
A painful swollen wound is red, warm, and no longer functions normally. Name the five cardinal signs of inflammation represented.
Answer: What are redness, swelling, heat, pain, and loss of function?
Explanation: These are the classic cardinal signs used clinically to recognize inflammation.
All three complement activation pathways eventually converge to generate a convertase for this central complement component.
Answer: What is C3?
Explanation: Classical, alternative, and mannose-binding lectin pathways begin differently but converge at C3 activation, eventually progressing to C5 activation and MAC formation
Name the one professional APC and the two semi-professional APCs identified in your material.
Answer: What are dendritic cells; macrophages; and B lymphocytes?
Explanation: Dendritic cells are classified as professional APCs, while macrophages and B lymphocytes are classified as semi-professional APCs.
A blood-film leukocyte has a U- or S-shaped nucleus with relatively parallel sides and lacks the distinct nuclear constrictions of a mature neutrophil. What cell is this?
Answer: What is a band neutrophil?
Explanation: Bands are immature neutrophils. The slides distinguish them from segmented neutrophils by their U/S-shaped nucleus and lack of distinct lobulation.
A dog has neutrophilia, lymphopenia, monocytosis, eosinopenia, and fewer than 1,000 bands/µL. Which leukogram pattern best fits?
Answer: What is a cortisol stress leukogram?
Explanation: The characteristic pattern includes mature neutrophilia with possible mild band increase, lymphopenia, monocytosis, and eosinopenia.
Acute inflammation occurs in three sequential phases. Put them in order.
Answer: What are fluidic → cellular → reparative?
Explanation: Acute inflammation is characterized initially by fluid/protein exudation, followed by leukocyte emigration—particularly neutrophils—and then repair/healing.
Match the trigger to the pathway:
Antibody-bound target
Mannose residues on a microbe
Activation on a microbial surface
Answer: What are classical, lectin, and alternative, respectively?
Explanation: The pathways differ primarily in their initiating events but ultimately converge on the same downstream complement cascade.
A macrophage engulfs an extracellular bacterial protein, processes it into peptide fragments, and prepares to show those peptides to a helper T cell. Which MHC molecule should carry the peptide?
Answer: What is MHC II?
Explanation: Professional and semi-professional APCs process engulfed extracellular proteins and load the resulting peptides onto MHC-II for presentation to helper T cells.
A bacterial infection causes a dramatic increase in tissue demand for neutrophils. To maintain the blood neutrophil count, which bone-marrow pool can rapidly release mature neutrophils?
Answer: What is the storage pool?
Explanation: Neutrophils progress through proliferation, maturation, and storage pools in the marrow. The storage pool contains mature cells available for release when inflammatory demand increases.
A febrile dog has:
WBC 27,700/µL
Segmented neutrophils 21,600/µL
Bands 4,600/µL
Lymphocytes 500/µL
2+ neutrophil toxic change
What leukogram pattern is most likely?
Answer: What is an acute inflammatory leukogram?
Explanation: This is the Heidi case from the lab. There is leukocytosis, neutrophilia, a substantial regenerative left shift, and toxic neutrophil change in an animal with clinical evidence of inflammation.
During acute inflammation, blood flow slows and leukocytes move from the central blood column toward the endothelial surface. Which step of leukocyte recruitment has occurred?
Answer: What is margination?
Explanation: The cellular-phase sequence is margination → rolling → activation/stable adhesion → transmigration toward a chemotactic stimulus.
Complement activation is normal through C5 cleavage, but the patient cannot assemble C5b through C9. Which major complement function is directly lost?
Answer: What is direct cell lysis by the membrane attack complex (MAC)?
Explanation: C5b initiates assembly of the terminal complement complex, C5b–C9, which produces direct membrane damage and lysis. C3b-mediated opsonization and C3a/C5a-mediated inflammatory effects occur upstream.
A virus is replicating inside a host cell, producing foreign proteins within that cell. The host cell displays fragments of those proteins to which major T-cell population?
Answer: What are cytotoxic T cells (CTLs)?
Explanation: Host infected cells contain foreign proteins produced internally and present peptide fragments derived from those proteins to cytotoxic T cells.
A neutrophil reaches inflamed tissue but cannot effectively ingest a bacterium. Complement activation is occurring normally, but the bacterium has not been adequately coated for recognition. Which complement fragment would normally improve this process?
Answer: What is C3b?
Explanation: C3b coats—or opsonizes—pathogens, enhancing their recognition and phagocytosis. Complement therefore doesn't only kill organisms directly through MAC.
Another severely ill patient has leukopenia, neutropenia, increased bands, and a degenerative left shift. What does this pattern tell you about tissue demand compared with the marrow's ability to supply mature neutrophils?
Answer: What is tissue demand is exceeding the bone marrow's ability to replenish mature neutrophils?
Explanation: This is the acute overwhelming inflammatory pattern. Unlike a typical acute inflammatory leukocytosis, mature neutrophils are being consumed faster than they can be replaced, producing neutropenia despite release of immature cells.
A biopsy from a lesion that has persisted for months contains macrophages, lymphocytes, plasma cells, proliferating fibroblasts, collagen deposition, and newly formed blood vessels. Is this acute or chronic inflammation, and what two repair processes are occurring?
Answer: What is chronic inflammation with fibrosis and angiogenesis/neovascularization?
Explanation: Chronic inflammation shifts away from predominantly neutrophilic inflammation toward mononuclear cells. Simultaneously, fibroblasts deposit collagen and new blood vessels form as part of granulation tissue and repair.
A bacterium avoids being coated with C3b but does not prevent formation of C3a or C5a. Which immune function would be most directly impaired: inflammation, chemotaxis, opsonization, or MAC formation?
Answer: What is opsonization?
Explanation: C3b is the major complement component emphasized for coating pathogens and enhancing phagocytosis. C3a and C5a are more closely associated with inflammatory recruitment, while C5b–C9 forms the MAC.
A dendritic cell successfully captures and processes a microbial antigen, but the appropriate T cell has a T-cell receptor that does not recognize the displayed peptide-MHC complex. Will that T cell be activated?
Answer: What is no?
Explanation: The T-cell receptor must specifically recognize the presented peptide and a portion of the MHC molecule. Simply displaying an antigen isn't sufficient if the responding T cell lacks the appropriate receptor specificity.
A genetic defect prevents neutrophil β2 integrins from interacting with ICAM-1 on activated vascular endothelium. The neutrophils can still move toward the vessel wall and roll normally. Which step of leukocyte recruitment fails?
Answer: What is stable adhesion?
Explanation: Margination occurs first, followed by selectin-mediated rolling. Activation increases integrin avidity, and β2 integrins such as Mac-1/CD11b-CD18 then bind endothelial ICAM-1 to produce firm adhesion. Without that interaction, the neutrophil cannot complete stable adhesion before transmigration.
Two dogs both have neutrophilia.
Dog A: lymphocytosis, no left shift, other leukocytes largely within reference intervals.
Dog B: lymphopenia, monocytosis, eosinopenia, and a mild band increase.
Neither pattern alone proves infection. Which leukogram is most consistent with catecholamine effects, and which with cortisol effects?
Answer: What are Dog A = catecholamine leukogram; Dog B = cortisol stress leukogram?
Explanation: Catecholamine leukograms characteristically include neutrophilia with lymphocytosis, whereas cortisol produces neutrophilia with lymphopenia, monocytosis and eosinopenia. This is why the entire leukogram should be interpreted rather than simply seeing neutrophilia and assuming inflammation.
Three animals experience similar tissue injury. One returns completely to normal. One develops a fibrous scar. The third develops a chronic granulomatous lesion around material that cannot be eliminated. According to the material, what three major factors help determine which outcome occurs?
Answer: What are severity of tissue damage, ability of the cells to regenerate, and biologic characteristics of the inciting agent or substance?
Explanation: Acute inflammation can resolve completely or progress to outcomes including chronic/granulomatous inflammation, fibrosis, increased cellularity, or abscess formation. The eventual outcome depends heavily on those three factors.
A mutation blocks C3 cleavage. Predict three downstream consequences of this single defect based on the major outcomes of the complement cascade.
Answer: What are reduced opsonization/phagocytosis, reduced inflammation/chemotaxis, and impaired MAC-mediated lysis?
Explanation: C3 activation sits at a critical convergence point. Without cleavage into C3a and C3b, C3b-mediated opsonization is lost, downstream C5 convertase formation is disrupted, and the cascade cannot normally progress to C5a generation and C5b–C9 MAC assembly.
Put these events in their correct sequence:
Generation of memory cells
Helper T-cell activation
B-cell and/or cytotoxic T-cell response
Antigen capture, processing, and presentation
Answer: What is antigen capture/processing/presentation → helper T-cell activation → B-cell and/or cytotoxic T-cell response → memory-cell generation?
Explanation: These are the four major steps of the adaptive immune response presented in the material. It begins with proper antigen presentation, progresses through helper T-cell activation and effector responses, and ends with generation of memory populations