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Parasitic protozoa

-single celled eukaryotes that replicate intracellularly (e.g. in RBCs) or extracellularity (e.g. in urine)


How microbes cause tissue damage

-direct invasion of cells resulting in cell death
-release of toxins that "kill at a distance" or enzymes that degrade tissue
-inducing host immune responses that cause tissue damage


Exotoxins secreted by bacteria

-enzymes (proteases, hyaluronidases)
-toxins that alter intracellular signally
-superantigens that stimulate large numbers of T cells, leading to massive cytokine release which can lead to shock


How can microbes evade the immune system?

-growth in niches that are inaccessible to the immune system (e.g. luminal intestine for C diff)
-antigenic variation (low fidelity of viral RNA polymerases such as in HIV; viral genome reassortment as in influenza)
-resistance to innate defenses (e.g. escaping phagocytosis; carbohydrate capsule on bacteria causing pneumonia shields antigens and presvents phagocytosis; some bacteria produce toxins that kill phagocytes or prevent their micration; neisseria etc secrete proteases that degrade antiobodies; some viruses produce proteins that block complement activation, e.g. herpes)
-impairment of effective T cell antimicrobial responses by specific or nonspecific immunosuppression (e.g. some DNA viruses bind to or alter localization of MHC class I proteins, impairing peptide presentation to CD8 cells)


Different inflammatory responses to infections

-purulent inflammation
-mononuclear infiltrates including granulomatous responses
-cytopathic/proliferation reactions (e.g. in viruses)
-tissue necrosis (e.g. c. perfringens)
-chronic inflammation and scarring


Histologic features of EBV

-striking paracortical area expansion by activated T cells (immunoblasts)
-minor population of infected B cells expressing EBNA2 and LMP1
-sometimes, EBV infected B cells resemble Reed-Sternberg cells
-sometimes, mild B cell follicular hyperplasia
-often, difficult to distinguish massive paracortical expansion from lymphoma


Examples of Staph virulence factors

-surface receptors for fibrinogen and other molecules to help it bridge to endothelial cells
-lipases to degrade lipids on skin surface
-alpha and beta toxins, that damage cell membranes
-A and B toxins which cause exfoliation resulting in a loss of barrier function
-superantigens that result in TSS (also found in strep pyogenes); these cause stimulation of T cells resulting in release of large amounts of cytokines that can result in shock


Examples of strep virulence factors

-capsules that resist phagocytosis
-M surface protein that prevents phagocytosis (probably antibodies to this result in rheumatic fever)
-S pyogenes secretes an exotoin that causes fever and rash


Anthrax morphology

-large, boxcar shaped gram positive extracellular bacteria in chains


Nocardia morphology

-filamentous gram positive bacteria that often have a beaded appearance due to irregular staining
-positive by Fite (modified acid fast) stain, unlike actinomyces


Donovan bodies

-Klebsiella granulomatis (Granuloma inguinale) in Giemsa smears; minute, encapsulated coccobacilli in macrophages; also positive with silver stain


Forms of leprosy

-tuberculoid: scaly skin lesions with decreased sensation (granulomas without bacilli)
-lepromatous: symmetric skin thickening and nodules with invasion into Schwann cells and macrophages with damage of peripheral nerves (granulomas with lots of bacilli in macrophages)
-good Th1 response results in tuberculoid form, while weak Th1 response, sometimes with a relatively increased Th2 response results in lepromatous form


What cells does CMV infect latently?

Monocytes and their bone marrow precursors


What genes does EBV express during latent infectino?

-EBNA1: binds EBV genome to chromosomes, permitting episomal persistence


Methods for diagnosing TB?

-conventional culture: takes 10 weeks but allows sensitivity testing for drugs
-liquid cultures: 2 weeks
-PCR: most rapid method


Three features of P. falciparum that make is more pathogenic than other subtypes?

-stimulates production of cytokines
-binds to RBCs of any age
-causes RBCs to clump together, resulting in ischemia