L 15 clinical ID Flashcards
Prions
Composed of modified host proteins (prion protein)
Cause transmissible spongiform encephalopathies
Associated with neurodegenerative diseases such as kuru, mad cow disease, Creutzfeldt-Jakob Disease (CJD).
Viruses
Obligate intracellular organisms
Dependent on host cell metabolism for replication
Classified by their nucleic acid content of their core and shape of their protein capsid or coat
Cause acute illnesses (colds, influenza)
Capable of lifelong latency and of long-term reactivation or of giving rise to chronic disease
Bacteriophages, Plasmids, Transposons
Mobile genetic elements that encode bacterial virulence factors
Include adhesins, toxins or enzymes that confer antibiotic resistance
They can infect bacteria and incorporate themselves into their genome (eg. Toxin genes of Vibrio cholerae and Corynebacterium diphtheriae)
Bacteria
Prokaryotes that lack nuclei and endoplasmic reticulum
Capable of synthesizing own DNA, RNA and proteins but rely on host for favorable growth conditions
Grow both extracellularly and intracellularly
characterists of Chlamydiae, Rickettsiae, Mycoplasmas
Obligate intracellular pathogens, divide by binary fission, susceptible to antibiotics, but lack certain cell structures
Chlamydiae
Can cause GU infections, conjunctivitis, respiratory infections & STDs
Rickettsiae
Rickettsiae: Transmitted by insect vectors (lice, ticks, mites) and can cause Rocky Mountain Spotted Fever, Q Fever, ehrlichiosis & scrub typhus
Mycoplasmas
Mycoplasmas: Tiniest free-living organism known and can cause atypical pneumonia & nongonococcal urethritis
Fungi
Possess thick cell walls
Growth patterns include budding yeast and slender tubes called hyphae
Hyphae produce fruiting bodies called conidia
Infect superficial layers of skin (Tinea)
Deep fungal infections can spread systemically (some species limited to geographic regions eg. Blastomyces, Histoplasma, Coccidioides)
Opportunistic fungi that normally colonize the body may cause disease in immunosuppressed patients such as lethal pneumonia & tissue necrosis
Prozoa
Parasitic, single-celled organisms with motility, pliable plasma membranes and complex cytoplasmic organelles
Can be transmitted:
sexually (Trichomonas)
via the fecal-oral route (Giardia)
by blood – sucking insects (Leishmania)
by contact with infected cats or eating cyst ridden, undercooked meat (Toxoplasma gondii)
Helminths
Parasitic worms that are highly differentiated multicellular organisms
Complex life cycles
Most are dependent on an intermediary host or vector for asexual reproduction
Disease is often caused by host inflammatory responses (ex. Schistosomiasis) and in proportion to the number of infecting organisms
3 classes of helminths
- Roundworms (nematodes): collagenous tegument non-segmented structure (hookworms & Trichinella)
- Flatworms (cestodes): gutless worms, heads sprout a ribbon of flat segments (tapeworms)
- Flukes (trematodes): primitive leaflike worms with syncytial integument (schistosomes)
Ectoparasites
Arthropods (lice, ticks, bedbugs, fleas)
Attach and live on skin
May be vectors for other pathogens such as deer ticks transmitting Lyme disease
HOW DO MICROORGANISMS CAUSE DISEASE
- Direct Cell Death
- Endotoxins/Exotoxins
- Secondary Through Host Immune Response
Mechanisms of Viral Injury
- Viruses inhibit host cell DNA, RNA or protein
synthesis. - Viral proteins insert into host cell’s plasma
membrane. - Viruses replicate efficiently and lyse host cells.
- Viral proteins on the surface of the host cells are
recognized by immune systems and host
lymphocytes attack the viral infected cells. - Viruses damage cells involved in secondary
infections. - Viral killing of one cell type causes the death
of another. - Slow virus infection and latency.
- In addition to causing injury, viruses induce cell
proliferation and transformation which can lead
to neoplasms.
Mechanisms of Bacteria-Induced Injury
- Bacterial Virulence
- Bacterial Adherence
- Bacterial Endotoxin
- Bacterial Exotoxins
Bacterial Adherence
a. Adhesins are bacterial surface molecules that bind to host cells (Fig. 8-2)
lipoteichoic acids, M proteins of S. pyogenes
Fimbriae or pili on surface of gram-negative bacteria
b. Entry into macrophages – directed by receptors that recognize antibodies or complement on surface of bacteria
c. Entry into epithelial cells – dependent on interactions between bacterial surface and epithelial cell receptor such as integrins
Bacterial Endotoxin
Lipopolysaccharide (LPS): structural component of outer cell wall in gram negative bacteria; induces host cytokine release to cause fever, activate macrophages & B cells
Bacterial Exotoxins
Toxins released by bacteria that interfere with cellular metabolism & allow bacteria to outgrow competing bacteria (ex. Diphtheria toxin, Vibrio cholera toxin, anthrax toxin)
Bacterial Virulence depends on
ability of bacteria to adhere, invade, & deliver toxic moieties
Ways microbes evade the immune system
- Being inaccessible to the immune response
- Resisting complement-mediated lysis and phagocytosis
- Varying or shedding antigens
- Causing specific & non-specific immuosuppression
types of inflammatory responses to infections
A. Suppurative (Polymorphonuclear) Inflammation
B. Mononuclear and Granulomatous Inflammation
C. Cytopathic-Cytoproliferative Inflammation
D. Necrotizing Inflammation
E. Chronic Inflammation and Scarring
Suppurative (Polymorphonuclear) Inflammation
Caused by pyogenic bacteria
Characterized by increased vascular permeability and leukocytic infiltration by neutrophils
Bacteria recruit neutrophils:
1. Directly by release of chemoattractive peptides
2. Indirectly by release of endotoxin which stimulates macrophages to release cytokines that chemoattract neutrophils
Mononuclear and Granulomatous Inflammati
Diffuse, predominantly mononuclear interstitial infiltrates form in response to pathogens
Include lymphocytes (syphilis chancres) and macrophages (mycobacterium granulomas) depending on the pathogen and host responses
Granulomatous inflammation occurs when aggregates of altered macrophages form or fuse to form giant cells
Cytopathic-Cytoproliferative Inflammation
Cytopathic-Cytoproliferative Inflammation
Reactions characteristic of virus-mediated damage to individual host cells in the absence of host inflammatory responses
Result in:
Inclusion bodies (CMV)
Polykaryons following cell fusion (measles)
Blisters due to cell damage (Herpesvirus)
Morphologic lesions (venereal warts/HPV)
Dysplastic changes & cancers
Necrotizing Inflammation
Rapid and severe tissue damage with predominant cell death in the absence of inflammatory infiltrates
Caused by uncontrolled viral infections, secreted bacterial toxins or cytolysis of host cells in protozoa infections (eg. Necrotizing fasciitis caused by Group A streptococcus)
Chronic Inflammation and Scarring
Chronic inflammation can lead to either complete healing or to extensive scarring
Several inert organism cause damage by the scarring response (ex. schistosome eggs)
