Microbiology: Gram Positive Bacilli Flashcards

1
Q

Commensal bacteria of the skin

A
  • Propionibacterium (+B, An)
  • Corynebacterium (+B, Ae)
  • Staphylococcus epidermidis (+C, Ae)
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2
Q

Commensal bacteria of the vagina

A

-Lactobacillus (+B, An)

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3
Q

Commensal bacteria of the oropharynx

A
  • Streptococcus (+C, Ae)
  • Haemophilus (-B, Ae)
  • Prevotella (-B, An)
  • Veillonella (-C, An)
  • Corynebacterium (+B, Ae)
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4
Q

Commensal bacteria of the GI

A

-Bacteroides (-B, An)

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5
Q

Pathogenesis of gram positive bacilli

A
  • GP do not produce endotoxins
  • Virulence factors can be acquired by plasmids or phage infection
  • Pathology from L immune evasion, toxin production, and secondary host response
  • Virulence factors: adhesins, exotoxins, exonzs, lysins
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6
Q

Exotoxins of GP bacilli

A
  • Expressed by both GP and GN bacilli
  • Responsible for most of the pathogenic effects of a given species
  • Can be either binary or non-binary
  • Are not needed for growth
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7
Q

Binary toxins

A
  • Expressed by GP and GN bacilli (acquired extrachromally, by phage or plasmid)
  • Have 2 domains, an A (activity) and B (binding)
  • B domain directs the toxin to a specific cell type by binding to the cell surface receptor
  • The A toxin then enters the cell to perform its function (often is ADP-ribosylating cellular targets)
  • The two domains can be encoded on the same gene or different genes
  • Cholera (-B) binary toxin inhibits Gs (GTP hydrolysis) pathway and activates AC
  • Diptheria (+B) binary toxin inhibits protein synthesis through ADP-ribosylation of eEF2
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8
Q

Diphtheria pathogenesis

A
  • Spread from person contact of Corynebacterium diptheriae (aerobic), with expression of diphtheria toxin (binary toxin)
  • This is normally found in oropharynx, pathogenic strains are infected w/ phage to express the toxin
  • Infection of tonsils and pharynx and is characterized by formation of a pseudomembrane, where the toxin is absorbed into the blood
  • Symptoms include malaise, sore throat, anorexia, fever
  • W/o Rx toxin can lead to prostration (extremely weak), rapid pulse, pallor, coma and death
  • Complications include myocarditis, neuritis (paralysis), respiratory insufficiency
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9
Q

Diphtheria diagnosis (Dx)

A
  • Based on clinical presentation (begin therapy w/o confirmatory cultures)
  • Identification is based on cultures: growth on Loeffler medium and variable gram staining of club-shaped bacilli
  • Is a reportable disease
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10
Q

Listeriosis

A
  • Caused by listeria monocytogenese, which is in soil and water and contaminates food products
  • Not infective to healthy adults but are to immunocompromised (IC), elderly, pregnant women, young children
  • Not killed by pasteurization, aerobic
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11
Q

Pathogenesis of Listeriosis

A
  • Grow intracellularly, produce LLO exotoxin (important for bacterial release from cells)
  • Is capable of cell-cell transfer
  • Internalin proteins allow entry into epithelia, uses the cell’s actin to move and “rockets” its way to neighboring cells (acquiring a double membrane)
  • Manifests in neonates by disseminated abscesses and granulomas early on
  • Later manifestation in neonates are meningitis or meningoencephalitis with sepsis
  • In susceptible adults symptoms are usually meningitis or acute febrile gastroenteritis
  • 20% mortality rate if untreated
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12
Q

Dx of listeriosis

A
  • Cultures of blood and CSF (GP coccobacilli)

- Reportable disease

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13
Q

Sporulation

A
  • Occurs in bacillus (GP aerobe) and clostridium (GP anaerobe) species
  • Normally grow thing (vegetative) cells begin sporulation after receiving signals from the environment
  • Spores have a complete copy of the genome, metabolically inert, resistant to most things
  • Germinate in presence of moisture and nutrients
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14
Q

Bacillus Anthracis life cycle

A
  • High untreated mortality (90-100%) of anthrax is due to its life cycle
  • Spores are the primary infectious agent depending on site of entry (cutaneous, GI, inhalation) but all forms of infection are life-threatening
  • Spores are phagocytosed and germinate in phagosomes of macrophages
  • Bacteria replicate intracellularly and are released after lysis of cell
  • They can escape immune system due to capsule
  • Exotoxin is produced at onset of bacteremia and is responsible for major pathogenic effects
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15
Q

B. Anthracis exotoxin

A
  • 2 types of binary toxins that share a same B domain (called PA, protective Ag)
  • EF (edema factor) or LF (lethal factor) are the possible A domains for PA
  • PA binds to cell membrane receptor and is cleaved by a protease, resulting in PA heptamerization (PA7) followed by binding of either LF or EF
  • Receptors for PA are TEM8 and CMG2 (ATRX1/2)
  • Once LF or EF bind to PA7, they are delivered into the cell
  • EF is an AC, leading to increased cAMP production (PKA), water efflux, loss of water homeostasis and cell death
  • LF is a Zn protease, w/ specificity for MAPK kinase1. Destruction of MAPK renders cell incapable of signal transduction. Leads to cell cycle disruption and cell death
  • LF has highest toxicity in cardiac/smooth muscle. EF has highest toxicity in liver
  • Used as bioweapon b/c: spores are effective dispersant, exotoxin has high lethality
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16
Q

Bacillus Cereus

A
  • Aerobic, widely found in soil and environment, often spread through contaminated food (causing gastroenteritis)
  • Can also infect penetrating wounds to the body (usually to eye)
  • GI irritation can be of early form ( emetic, or food poisoning) and late form (diarrheal)
  • Can become septic in IC patients
17
Q

B Cereus emetic disease

A
  • Symptoms are abdominal pain/discomfort, nausea, vomiting. These appear quickly (1-8 hrs) and resolve in a day
  • Usually due to improperly cooked foods
  • Bacteria contamination of foods leads to enterotoxin secretion, and subsequent toxin contamination of the food (pre-formed toxins)
  • These enterotoxins are heat-stable and are not destroyed upon cooking, therefore killing the bacteria with cooking will still lead to intoxication and irritation of upper GI
18
Q

B Cereus diarrheal disease

A
  • Takes up to 24 hrs to appear, due to bacterial outgrowth in lower GI (from vegetative cells and spores)
  • Symptoms are abdominal discomfort (pain/cramps) and diarrhea
  • Absence of vomiting is noteworthy
  • Growth of cells in colon leads to localized enterotoxin production, causing the diarrhea