Infectious Disease Transmission Flashcards

1
Q

Describe prions

A

Protein particles without a genome. Infectious and capable of producing disease. Ex: Creutzfeldt-Jakob disease, Kuru and “mad cow” dz. Slow neurodegenerating diseases

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2
Q

Describe viruses

A

Intracellular pathogen/incapable of replication outside a living cell. Consist of a protein coat (capsid), surrounding either RNA or DNA. Viruses MUST penetrate a susceptible living cell & use the biosynthetic machinery of the cell to produce viral progeny (Latency). ONCOGENIC: HPV, Epstein-Barr

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3
Q

Describe bacteria

A

Autonomously replicating unicellular organism (prokaryotes). contain no organized intracellular organelles. Genome consists of a single chromosome of DNA and RNA. Most produce asexually by cellular division. Gram-positive—PURPLE. Gram-negative—RED

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4
Q

Describe fungi

A

Free-living, eukaryotic saprophytes found in every habitat on earth. serious fungal infections are rare. Reproduction is sexual or asexual (Involves production of spores). separated into two groups: yeasts and molds

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5
Q

What are the differences between yeasts and molds?

A

Yeasts: Single-celled organisms, Reproduce by a budding process, Colonies are smooth with a waxy or creamy texture. Molds: Produce long, hollow, branching filaments—hyphae. Some produce cross walls which segregate the hyphae. Produce cottony or powdery colonies of mats of hyphae–mycelium

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6
Q

What are arthropods?

A

parasitic vectors such as ticks, mosquitoes, biting flies.

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7
Q

What are ectoparasites?

A

Infest external body surfaces and cause localized tissue damage or inflammation secondary to the bit or burrowing action (Mites (scabies), Chiggers, Lice, Fleas)

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8
Q

What are protozoa?

A

Unicellular parasites with eukaryotic machinery**. Reproduction may be sexual or asexual. Most are saprophytes, but some can cause disease in the human. Ex: amebic dysentery, malaria, and giardiasis

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9
Q

What are helminths?

A

Collection of wormlike parasites: nematodes (roundworms), cestodes (tapeworms), & trematodes (flukes). Often an intermediate host is required for development & maturation of the offspring and then humans are infected and sexual reproduction occurs in the human host. Helminth infections often involve multiple organ systems

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10
Q

What is the difference between incidence and prevalence?

A

Incidence—number of new cases. Prevalence—number of active cases at any given time

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11
Q

What are exotoxins?

A

Proteins released from the bacterial cell DURING growth. Enzymatically inactivate or modify cellular constituents, leading to cell death or dysfxn (diptheria, botulism, toxic shock syndrome). produce vomiting/diarrhea—enterotoxins (E. coli 0157:H7)

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12
Q

What are endotoxins?

A

molecules composed of lipid & polysaccharides found in the cell wall of gram-negative bacteria. NOT actively released during growth of the bacteria & have no enzymatic activity. They are potent activators of regulatory systems (induce clotting, hypotension, fever). Can induce endotoxic shock

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13
Q

Describe how pathogens use adhesion factors

A

Site to which a microorganisms adheres to is called a RECEPTOR where there is a LIGAND or ADHESIN. After initial attachment, a number of bacterial agents embed into a gelatinous matrix of polysaccharides (flu, mumps, measles)

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14
Q

Describe how pathogens use evasive factors

A

Polysaccharides (capsules, slime, & mucous layers) discourage engulfment & killing by the phagocytic WBCs. Some organisms secrete toxins that deplete the hosts WBCs. Some pathogens can survive INSIDE the ingestion by the WBC.

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15
Q

What are some specific examples of pathogens using evasive factors?

A

S. aureus secretes coagulase that causes blood to clot around the pathogen & protects it from phagocytosis. H. pylori produces urease that converts gastric urea into ammonia which neutralizes the acidity of the stomach allowing the pathogen to survive. H. influenzae & N. gonorrhoeae secrete enzymes that inactivate IgA

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16
Q

Describe how pathogens use invasive factors

A

Products produced by infectious agents that facilitate penetration of anatomic barriers & host tissue

17
Q

What determines empirical antibiotic therapy?

A

location of the infection, the most likely pathogens that infect that location, the setting where the infection occurred, and known community resistances

18
Q

How do bacteria become resistant to PCNs/cephalosporins?

A

Inactivation of the drug by beta-lactamases (enzymes) due to acquired plasmid insertions or direct DNA mutations. To overcome resistance add a beta-lactam inhibitor. Bacteria can also decrease penetration to the target site (gram-negative bacteria) or alter the binding site (penicillin-binding-proteins—PBPs).

19
Q

How do bacteria become resistant to sulfonamides?

A

Overproduction of PABA. Structural changes in enzymes so there is less affinity for the sulfonamide substrate. To overcome resistance typically use in combination w/ other agents (trimethoprim)

20
Q

How do bacteria become resistant to fluoroquinolones?

A

Chromosomal mutations: active efflux of the drug or protection of DNA gyrase. Alterations in their ability to permeate the bacterial cell wall.

21
Q

How do bacteria become resistant to macrolides?

A

Alterations in the macrolide binding site on the ribosomal subunit. Altered transport of the macrolide

22
Q

What are common opportunistic infections and their locations?

A

Brain- toxoplasmosis, cryptococcal meningitis. Eyes- CMV. Mouth/throat- candidiasis. Lungs- pneumocystis carinii pneumonia, TB, histoplasmosis. Gut- CMV, cryptosporidiosis, mycobacterium avium complex. Skin- HSV, shingles. Genitals- HSV, HPV, candidiasis