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Pathogenic Microbiology > Test 2 > Flashcards

Test 2 Flashcards

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1
Q

Describe mycobacteria

A

Nonmotile, non-spore forming, aerobic, gram positive, acid fast due to long mycolic acid chains, slow growing

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2
Q

What is the best way to tell tuberculosis mycobacteria from nontuberculous mycobacteria

A

Tuberculosis bacteria are either nonpigmented or a light tan color, whereas NTM are yellow carotenoids

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3
Q

Generally describe Mycobacterium tuberculosis

A

An intracellular pathogen, enters respiratory airways to infect the alveolar macrophages

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4
Q

What diseases are caused by MAC and what are they?

A

Lady Windermere Syndrome: Occurs in elderly women who hold in their cough, which causes inflammation to increase and predisposes them to superinfection with MAC

Old man smoking disease: they deserve it

Solitary pulmonary nodule: MAC is the most common cause of these nodules

Any and all of these diseases are particularly dangerous to immunocompromised/HIV/AIDS patients

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5
Q

How does M. tuberculosis spread disease and cause damage to the body?

A

It prevents fusion of the phagosome with lysosomes, which causes the lysosome to fuse with other intracellular vesicles to facilitate intracellular replication

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6
Q

Describe the transmission of M. tuberculosis and who is most at risk for the bacterial disease

A

Humans are the only natural reservoir for the bacteria, but it is spread by close person to person contact; it is dangerous for homeless people, prisoners, immunocompromised, and HIV patients

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7
Q

How should Mycobacteria tuberculosis infections be treated?

A

Multiple antibiotics should be given for an extended period: rifampin is commonly used; vaccination with attenuated BCG can be used to help stop the spread of disease

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8
Q

What are the symptoms of TB and how is a Mycobacterium tuberculosis infection diagnosed?

A

Malaise, weight loss, cough with or without blood

It is diagnosed by X-ray scans of the lungs, positive skin reactivity, and the laboratory detection of mycobacteria

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9
Q

Generally describe actinomyces

A

Facultatively anaerobic or strictly anaerobic gram positive rods, non acid fast, slow growing, naturally inhibit the upper respiratory, GI, and female genital tracts

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10
Q

What are the diseases caused by actinomyces?

A

Actinomycosis: The development of chronic granulomatous lesions that form abscesses; often form sulfur granules
Cervicofacial infections: Infections of the face/mouth due to poor oral hygiene or invasive dental procedures

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11
Q

How should infections of actinomyces be diagnosed and treated?

A

Cultures should be collected from the sulfur granules if possible (since contamination can occur from mucus membranes)

Treatments include prolonged administration of penicillin or carbapenems; good oral hygiene can also help reduce the risk

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12
Q

Describe Nocardia

A

Strict aerobic rods, form branched aerial hyphae, gram positive, weakly acid fast, slow growing, catalase positive, found in soil rich with organic matter, and can survive/replicate in macrophages by preventing fusion of the phagosome/lysosome (mediated by the cord factor)

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13
Q

How do Nocardia avoid being killed by the immune system?

A

They avoid phagocytic killing through secreting catalase and superoxide dismutase (which break down the toxic oxygen metabolites released by phagocytes)

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14
Q

What are the diseases caused by Nocardia?

A

Bronchopulmonary disease: Indistinguishable from infections by other pyogenic organisms, but develops more slowly; a immunological defect is usually assumed

Cutaneous infections: Can be primary (mycetoma, cellulitis, subcutaneous abscesses) or secondary due to spreading or organisms

Mycetoma: A painless, chronic infection of the feet (subcutaneous swelling of the muscles, tissues, and bone; suppuration; multiple sinus tracts form)

Lymphocutaneous infections: Cutaneous nodules and ulcerations along the lymphatics and regional lymph node involvement

Can also cause: chronic ulcerative lesions, subcutaneous abscesses, cellulitis, and brain abscesses

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15
Q

How should you diagnose and treat Nocardia infections?

A

Take multiple sputum samples to test by microscope, grow on buffered charcoal yeast extract agar (BCYE), analyze rRNA genes

Treat by TMP-SMX, broad-spectrum cephalosporins, prolonged treatment of ABs to prevent relapses, and providing proper wound care

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16
Q

Briefly describe Rhodococcus

A

Gram positive, acid fast bacteria, initially appear rodlike but then revert to coccoid forms, are salmon pink after about 4 days of growth, and slow growing

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17
Q

Describe Rhodococcus equi and the diseases it can cause

A

Facultative, intracellular organism that survives in macrophages to cause granulomatous inflammation that leads to abscess formation

Causes invasive pulmonary disease (immunocompromised patients) and opportunistic infections (immunocompetent patients)

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18
Q

How should Rhodococcus infections be treated?

A

Infections in immunocompromised patients should include 2+ antibiotics, including one with activity in macrophages; penicillins should not be used

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19
Q

Generally describe Mycobacterium leprae

A

Spread by person to person contact, release lepromin as the antigen, non acid fast, and cannot grow in cell-free cultures

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20
Q

What are the two phases of leprosy?

A

Tuberculoid leprosy: Strong cellular immune response, hypopigmented skin macules, reactive skin tests to lepromin

Lepromatous leprosy: Strong antibody response, defect in cellular response, more infectious form, disfiguring skin lesions, nodules, plaques, thickened dermis, etc.

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21
Q

How should the two forms of leprosy be treated?

A

Tuberculoid: Rifampicin and dapsone for 6 months minimum

Lepromatous: Clofazimine + rifampicin + dapsone for 1 year

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22
Q

What is the Mycobacterium avium complex (MAC)?

A

The most common pathogenic acid-fast species, including M. avium and M. intracellulare

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23
Q

How should you treat a disease caused by MAC?

A

Clarithromycin or azithromycin combined with ethambutol and rifampin; the individual treatment depends on the response to therapy

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24
Q

Briefly describe non-tuberculosis causing mycobacterium

A

Can be split up into slow growing and fast growing; rapidly growing species have lower virulence potential (and are more susceptible to antibiotics) and are usually only infectious when introduced into an open wound (wound dressings, heart valves, etc)

Treat by removing prosthetic devices and by cefoxitin/sulfonamides

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25
Q

Generally describe Neisseria as a genus

A

Gram negative, aerobic, coccoid shaped in diplococci pairs with a flattened side, oxidase positive, catalase positive, acid produced in carbohydrate presence, and non motile

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26
Q

Describe the special properties of Neisseria Gonorrhoeae

A

Only grows on enriched chocolate agar and other supplemented media, 37 degrees is the optimum TM, humid atmosphere with 5% CO2 is required or enhances growth, colonized mucosal surfaces (humans are only reservoir), susceptible to drying, cooling, and fatty acids, and produces acid from glucose but not other sugars

27
Q

What are the clinical symptoms of meningitis?

A

Headache, fever, neck pain, presence of Neisseria meningitisis in the blood and spinal fluid, etc

28
Q

How is Neisseria meningitidis diagnosed?

A

A gram stain is very sensitive and specific, antigen detection is not recommended, nucleic acid based tests are extremely useful, and Thayer-Martin medium is selective for N. meningitidis

29
Q

What treatment is recommended for N. meningitidis infections?

A

Cefotaxime or ceftriaxone should be used; a polyvalent vaccine exists against the serogroups of N. meningitidis

30
Q

Generally describe Candida as a genus

A

Gram negative diploid eukaryotic fungus, can potentially undergo phenotypic switching between yeast-like form and hyphal form; only natural reservoir is humans, common in GI tract and mouth

31
Q

Where do Candida albicans infections come from and how do they spread?

A

Infections can be endogenous (from commensal flora) or exogenous from contaminated solutions, hospital tools, etc.

32
Q

What diseases does Candida albicans cause?

A

Blood stream infections, genital, cutaneous, and oral infections, invasive systemic infections, etc.

33
Q

How are Candida albicans infections diagnosed?

A

Cultures can be plated on YPD or CHROMagar for detection of mixed species; skin lesions or scrapings can also be investigated for cultures

34
Q

How do you treat Candida albicans infections?

A

Azole antifungals, amphotericin B, fluconazole, and caspofungin; there is no approved vaccine yet

35
Q

What are the virulence factors for Candida albicans?

A

Cell wall proteins (adhesins), enzymes (lipases, etc), and candidalysin (peptide that acts as a toxin to lyse RBCs)

36
Q

Generally describe Cryptococcus

A

Systemic mycosis, encapsulated yeastlike fungi, often present in soil and pigeon poop

37
Q

How would a Cryptococcus neoformans infection be diagnosed?

A

Staining with India ink shows the capsules, the cells can be seen in blood or CSF samples, and detection of the polysaccharide antigen is very vital

38
Q

How is Cryptococcus neoformans treated?

A

The meningitis infection is deadly without treatment, amphotericin B followed by fluconazole is the the treatment for relieving brain pressure

39
Q

What are the major classes of antifungals and how do they work?

A

Azoles: inhibit 14-alpha-demethylase to cause toxic sterols to accumulate in the membrane rather than ergosterol (causes enhanced membrane permeability and cell death)

40
Q

What is the Enterobacteriaceae family?

A

Medically important gram negative rods found in soil, water, vegetation, and intestinal flora

41
Q

Describe the characteristics of the Enterobacteriaceae family

A

Gram negative rods, non spore forming, most of them are motile, facultative anaerobes, ferment glucose, reduce nitrate, catalase positive, oxidase negative, and all of them have an enterobacterial common antigen

42
Q

What are some of the methods to differentiate between Enterobacteriaceae?

A

Lactose fermentation, resistance to bile salts, and presence of capsules versus slime layers

43
Q

What Enterobacteriaceae ferment lactose and which ones do not?

A

Lactose non- fermenting:
Salmonella, Shigella, Yersinia, and Proteus (PYSS)

Lactose fermenting:
Escherichia, Klebsiella, Enterobacter, Citrobacter, and Serratia (SCEEK)

44
Q

What is the major cell wall antigen for Enterobacteriaceae and what are its components?

A

The heat-stable lipopolysaccharide (LPS); its components are the outermost O polysaccharide (vital for classification), a core polysaccharide, and lipid A (endotoxin activity)

45
Q

What are the three major groups of antigens by which Enterobacteriaceae are grouped?

A

Somatic O polysaccharides, K antigens (capsule antigen), and H proteins (flagella antigen)

46
Q

What virulence factors do the Enterobacteriaceae have?

A

Endotoxins depending on Lipid A component of LPS, capsule (if present), antigenic phase variation of O, K, and H antigens based on expression, type 3 secretion systems, growth factor sequestration, serum killing resistance, and antimicrobial resistance

47
Q

What are type 3 secretion systems?

A

A system for delivering virulence factors into eukaryotic cells; think of it as a molecular syringe of 20 proteins that push virulence factors into a cell

48
Q

Describe Escherichia coli by virulence factors, diseases it causes, and any special attributes

A

Virulence factors: Adhesins and exotoxins

Diseases: Commensal organisms that can then cause disease, sepsis, UTIs, hospital acquired infection, and gastroenteritis

Special attributes: There are 5 strains of E. coli that can cause gastroenteritis

49
Q

What are the 5 strains of E. Coli that can cause gastroenteritis and how do you tell them apart?

A

Enterotoxigenic E. coli (ETEC): acquired by food or water, causes secretory (non bloody) diarrhea, produces a heat stable and heat-labile toxin

Enteropathogenic E. coli (EPEC): Have a locus of enterocyte effacement (LEE), have an E. coli adherence factor (EAF) plasmid, bacteria attaches to epithelial cells of small intestine and then microvillus, causes non bloody diarrhea

Enteroaggregative E. coli (EAEC): Causes chronic diarrhea and growth retardation in children

Enterohemorrhagic/Shiga toxin-producing E. coli (EHEC/STEC): Shows presence of Shiga toxin 1 or 2 that inhibits protein synthesis, causes bloody diarrhea

Enteroinvasive E. coli (EIEC): Watery diarrhea, invasive plasmid antigen, releases hemolysin

Uropathogenic (UPEC) E. coli: Have P pili and fimbriae to attach to the urogenital tract

50
Q

Describe Salmonella by virulence factors, diseases it causes, and any special attributes

A

Virulence factors: Type III Secretion System and Pathogenicity Islands I and II (intestinal epithelium entry versus intracellular bacteria replication)

Diseases: Septicemia, Gastroenteritis, and Enteric Fever

Special attributes: Attaches to the small intestine and invades M cells to replicate

51
Q

Differentiate between the two types of Salmonella

A

Typhoidal (enteric): Restricted to growth in human hosts, causes typhoid and paratyphoid fever, lives in GI tract and bloodstream, usually S. typhi

Nontyphoidal Salmonella: Causes principally gastroenteritis, usually transmitted animal-to-person through food products, generally self-limiting, usually S. enteritidis or S. typhimurium

52
Q

What are the symptoms of salmonella illnesses and how are they treated?

A

Symptoms: Nausea, vomiting, non-bloody diarrhea, fever, or abdominal cramps

Treatment: Generally no treatment since the disease will resolve on its own, salmonella vaccines are applied to baby chicks via drinking water, and humans can have one of 3 vaccines for Salmonella (inactivated whole cell, live and attenuated, or Vi polysaccharide vaccine)

53
Q

Describe Shigella by virulence factors, diseases it causes, and any special attributes

A

Virulence factors: Type III secretion system of IpaA-D proteins, large virulence plasmid (T3SS genes on pWR100), replication in the cytosol after lysing the phagocytic vacuole, and Shiga toxin (A subunit and 5 B subunits)

Diseases: Shigellosis

Special attributes: Humans are only reservoir, transmitted between people and usually from pediatric caregivers

54
Q

How is Shigellosis diagnosed and how is it treated?

A

Abdominal cramps, diarrhea, fever, bloody stools, mucus in stool

Antibiotics limit spread to household, include Ampicillin, Fluoroquinolone, and Trimethoprim

55
Q

Describe Yersinia by virulence factors, diseases it causes, and any special attributes

A

Virulence factors: Resist phagocytic killing by Type III secretion system, the fraction 1 gene for an antiphagocytic protein capsule, and a plasminogen activator protease gene to degrade complement components

Diseases: Zoonotic, the sylvatic plague and the urban (black) plague are big ones; bubonic plague and pneumonic plague

Special Attributes: Difficult to eradicate since there are reservoirs in fleas, rats, cats, etc., intracellular growth in macrophages, can grow at 4 degrees

56
Q

What are the symptoms of Bubonic plague and pneumonic plague? How are they treated?

A

B. plague symptoms: 7 days incubation period after flea time, high fever, painful bubo (swelling of lymph nodes), bacteremia develops rapidly

P. plague symptoms: 2-3 day incubation period, fever, malaise, pulmonary signs, person to person spread by aerosols

Treatment: Tetracyclines, Chloramphenicol, Sulfa drugs, vaccines of killed bacilli are short term protective, and immunity is good if you survive

57
Q

Describe Klebsiella by virulence factors, diseases it causes, and any special attributes

A

Virulence factors: Prominent capsule

Diseases: Lobar pneumonia, wound infection, soft-tissue infection, and UTIs

Special attributes: Mucoid appearance, doesn’t cause GI disease even though it’s found there, becoming increasingly resistance to antibiotics

58
Q

Describe symptoms and treatment of Lobar Pneumonia from Klebsiella species

A

Symptoms: Blood tinged sputum, formation of cavities (in the lungs?), and necrotic destruction of alveolar spaces

Treatment: Not fucking B-lactams, they’re super resistant

59
Q

Describe Proteus by virulence factors, diseases it causes, and any special attributes

A

Virulence factors: Urease

Diseases: UTIs, cystitis, pyelonephritis (?), kidney stones

Special attributes: Raise pH of urine due to urease (increase Ca and Mg), fimbriae attach it to the uroepithelial cells

60
Q

Describe Vibrio by virulence factors, diseases it causes, and any special attributes

A

Virulence factors: Pili like the toxin coregulated pilus (TCP), the Vibrio Pathogenicity Island (VP1-1) along with bacteriophage CTXO encodes for the heat-labile cholera toxin, chemotaxis proteins, and enterotoxins that can work without the cholera toxin

Diseases: Cholera, gastroenteritis, primary septicemia, and wound infection

Special attributes: Require sodium chloride for growth,

61
Q

Generally describe the Vibrio genus

A

Curved rods, broad growth temperature range, require sodium chloride (halophile), susceptible to stomach acids, polar flagella, cell wall with lipopolysaccharides made of lipid A (endotoxin), Core polysaccharide, and an O polysaccharide that is specific to each serogroup, grow in estuarine and marine environments, form symbiotic association with chitinous shellfish (reservoir)

62
Q

Explain how the cholera toxin is transmitted into a cell and what it does to the host

A

The Bacteriophage CTX O encodes ctxA and ctxB cholera toxin subunits (AB toxin); the B subunit binds to GM1 receptors and the A subunit binds to regulator complexes and activates cAMP, leads to a severe loss of fluids/electrolytes, also causes blocking of sodium and chloride uptake in the small intestine

63
Q

What are the symptoms and treatment of cholera?

A

Symptoms: Severe “rice-water” diarrhea 2-3 days after injection of contaminated food/water, muscle cramps, cardiac arrhythmia, and renal failure

Treatment: Rehydration during illness is crucial, water purification, sanitation, and sewage treatment is helpful to prevent outbreak, subunit B vaccines and inactivated whole cell vaccines exist but are not effective long term

Pathogenic Microbiology (4 decks)

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