9-30 Microbiology Review 2 Flashcards

1
Q

What kind of germ is Legionella pneumophila?

A
  • Weakly gram-negative pleomorphic rod
  • Facultative intracellular
  • Requires cysteine and iron ( Charcoal yeast extract)
  • Water organism, amebae, air-conditioning water cooler tanks
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2
Q

What is the transmission for Legionella pneumophila?

A

•aerosols from contaminated air-conditioning, no human to human transfer

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3
Q

What are some risk factors for Legionella pneumophil infection?

A

•smokers over age 55 with high alcohol intake and immunosuppression

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4
Q

What are the diseases that result from Legionella pneumophila?

A

Legionaire’s disease

Pontiac fever

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5
Q

What is the clinical presentation of Legionaire’s disease?

A
  • Fevers, malaise, cough, chills , dyspnea, myalgias, headache, chest pain, and diarrhea.
  • Myalgias, severe headaches, and diarrhea distinguish it from other pneumonias
  • Mental Confusion
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6
Q

What is the clinical presentation of Pontiac fever?

A
  • Fever, sore throat myalgia, headache, and extreme fatigue
  • Short duration, lasting on average 3 days
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7
Q

How is an infection with Legionella pneumophila Dx’ed?

A
  • Antigen urine test
  • DFA ( direct fluorescent antibody)
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8
Q

How is an infection with Legionella pneumophila treated?

A
  • Fluoroquinolones, azithromycin, or erythromycin + rifampin for immunocompromised patients
  • Drug must penetrate human cells
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9
Q

What kind of germ is Mycoplasma pneumonia? What does it need for culture?

A
  • Smallest free-living bacteria
  • No cell wall – unaffected by cell-wall inhibiting antimicrobials such as B-lactams
  • Sterol containing membrane
  • Requires cholesterol for culture
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10
Q

What kind of transmission happens with Mycoplasma pneumonia?

A
  • Transmission: respiratory droplets, close contact, families, military recruits, dorms
  • Highest incidence age 5-20 years old
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11
Q

What is the clinical presentation of infection with Mycoplasma pneumonia?

A
  • Respiratory Infection
  • 2-3 weeks incubation
  • Fevers, malaise, headache, and cough
  • 5-10% progress to tracheobronchitis or pneumonia
  • Cough usually non-productive
  • Walking pneumonia
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12
Q

How is an infection with Mycoplasma pneumoniae Dx’ed?

A
  • Primarily clinical diagnosis
  • Positive cold agglutinins - positive in 65% of cases
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13
Q

How is an infection with Mycoplasma pneumoniae treated?

A
  • Macrolides: erythromycin, azithromycin, and clarithromycin
  • Tetracyclines
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14
Q

What kind of germ is Streptococcus pneumonia? What does it need to grow?

A
  • Gram positive diplococcus, lancet shaped
  • Facultative anaerobe, grows on blood agar plates
  • alpha hemolytic
  • Optochin sensitive
  • Lysed by bile
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15
Q

What is the reservoir for Streptococcus pneumonia?

A

•human upper respiratory tract

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16
Q

How is Streptococcus pneumonia transmitted?

A

respiratory droplets

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17
Q

What is the pathogenesis factor for Streptococcus pneumonia?

A

•Polysaccharide capsule

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18
Q

What are the risk factors for contracting a Streptococcus pneumonia infection?

A

•Influenza infection, COPD, CHF, Alcoholism, and asplenia

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19
Q

How does Streptococcus pneumonia initially colonize a host?

A

•Initially colonizes the nasopharynx then aspirated

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20
Q

What are the clinical manifestations of Streptococcus pneumonia infection?

A

Typical pneumonia

Adult meningitis

OM and sinusitis

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21
Q

What are the clinical signs and symptoms of the diseases caused by Streptococcus pneumonia?

A
  • Typical Pneumonia
  • Most common cause
  • Shaking chills, high fever, chills, rigors, lobar consolidation, blood tinged (rusty) sputum
  • Adult meningitis
  • Most common cause in adults
  • Otitis media and sinusitis
  • Most common cause in children
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22
Q

How is pneumonia caused by Streptococcus pneumonia treated?

A
  • Beta lactams
  • Macrolides
  • Fluoroquinolones
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23
Q

How is meningitis caused by Streptococcus pneumonia treated?

A
  • Treatment of meningitis:
  • 3rd generation cephalosporins
  • Vancomycin added if penicillin resistant
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24
Q

What kind of germ is Staphylococcus aureus? What does it need to grow on culture?

A
  • Gram positive cocci in clusters
  • Catalase positive
  • Coagulase positive
  • Beta hemolytic
  • Small yellow colonies on blood agar
  • Ferments mannitol
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25
Q

What is the most common reservoir for Staphylococcus aureus?

A

•nasal flora in 25% of population

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26
Q

What is the typical transmission for Staph. aureus? Why is it disgusting to sneeze into your hands?

A
  • Transmission:
  • Hands
  • Sneezing
  • Surgical wounds
  • Contaminated food:
  • Custards
  • Potato salad
  • Canned meats

Sneezing - see above. Sneeze into your elbow, don’t be gross!

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27
Q

What are the virulence factors associated with Staphylococcus aureus?

A
  • Over 50 virulence factors including adhesins, toxins, enzymes, surface-binding proteins, and capsule polysaccharides
  • Pathogenesis from tissue invasion and toxin mediated
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28
Q

What are the toxin mediated disease with Staphylococcus aureus?

A
  • 3 toxin mediated diseases:
  • Staphylococcal food poisoning
  • Staphylococcal toxic shock syndrome
  • Staphylococcal scalded skin syndrome
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29
Q

What are the skin-related clinical manifestations of Staphylococcus aureus infection?

A

•Skin manifestations include impetigo, folliculitis, furuncle, abscess, erysipelas, cellulitis, mastitis, necrotizing fasciitis, and wound infections

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30
Q

What are the systemic and organ-related clinical manifestations of Staphylococcus aureus infection?

A
  • Bacteremia
  • Endocarditis
  • Roth’s spots, Osler’s nodes, Janeway lesions, and petichiae
  • Pericarditis
  • Osteomyelitis – hematogenous seeding
  • Septic Arthritis, Infected prosthetic joints
  • Pneumonia – nosocomial pneumonia, salmon colored sputum
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31
Q

What are the clinical manifestations of staphylococcal food poisoning?

A
  • 2-6 hours after eating nausea, vomiting, diarrhea, and abdominal pain
  • Self limited
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32
Q

What are the clinical manifestations of Toxic Shock Syndrome? What is the responsible agent?

A
  • Toxic Shock Syndrome - TSST-1 a super antigen is major cause
  • Fever, erythroderma, hypotension, involvement of 3 or more organ systems, and desquamation of the palms and soles
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33
Q

What is the virulence factor behind Scalded Skin Syndrome?

A

•exfoliative toxin A or B

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34
Q

What is the treatment for Staph. aureus infection?

A
  • Gastroenteritis is self limiting
  • Nafcillin/Oxacillin
  • MRSA – Vancomycin
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35
Q

What kind of a germ is Pneumocystic jiroveci? What is needed to visualize this?

A
  • Fungus
  • Obligate extracellular parasite
  • Silver stain
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36
Q

What kinds of patients end up with infections of Pneumocystis jiroveci?

A

•Opportunistic infection in HIV patients with CD4 count less than 200

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37
Q

What are the clinical manifestations of a Pneumocystis jeroveci infection?

A
  • Pneumonia
  • Fever, nonproductive cough, and shortness of breath
  • X-ray with patchy infiltrate, ground glass appearance, lower lobe and periphery may be spared
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38
Q

How is pneumonia caused by Pneumocystis jeroveci Dx’ed?

A

silver staining cysts in bronchial alveolar lavage fluids or biopsy

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39
Q

How is pneumonia due to Pneumocystic jeroveci treated?

A

•sulfamethoxazole/trimethoprim or dapsone

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40
Q

How is infection by Pneumocystis jeroveci prevented?

A

•Prevention SMX/TMP prophylaxis for CD4 counts less than 200 in HIV patients

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41
Q

What kind of germ is Histoplasma capsulatum? Where is it found?

A
  • Dimorphic fungus
  • Facultative intracellular parasite – found in RES cells
  • Found in soil, caves, and abandoned buildings with bird and bat guano
  • Endemic to Mississippi and Ohio River Valleys
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42
Q

How is Histoplasma capsulatum transmitted?

A

•Disruption of soil; cleaning attics, bridges, and barns; tearing down old structures, and spelunking

43
Q

What are the clinical manifestations of Histoplama capsulatum infection?

A
  • Acute pulmonary
  • Most asymptomatic
  • Several weeks after exposure fevers, chills, fatigue, non-productive cough, anterior chest discomfort, and myalgias
  • Chronic pulmonary
  • Progressive, often fatal
  • Elderly, immunocompromised, and COPD patients at risk
44
Q

How is an infection with Histoplasma capsulatum Dx’ed?

A
  • X-ray
  • Acute Pneumonia with patchy lobar or multilobar infiltrate
  • Chronic Pneumonia with upper lobe infiltrates, multiple cavities, fibrosis of lower lobes – mimics TB
45
Q

How is a Histoplasma capsulatum infection treated?

A
  • Itraconazole
  • Amphotericin B
46
Q

What kind of germ is Blastomyces dermatitidis? Where is it found?

A
  • Thermally dimorphic fungus
  • Broad based budding yeast
  • Appears to be associated with soil and decaying vegetation, especially in areas associated with rivers and lakes.
47
Q

Where is Blastomyces dermatitidis endemic?

A

•Endemic in north central, south central, great lakes, and southeastern seaboard

48
Q

How is Blastomyces dermatitidis transmitted?

A

inhaled conidia

49
Q

What are the clinical manifestations of an acute Blastomyces dermatitidis infection?

A
  • Acute Pulmonary
  • Most asymptomatic or thought to have community acquired pneumonia
  • Fever, malaise, nonproductive cough
  • Chest x-ray with lobar, multilobar, or nodular infiltrates
  • Skin lesions
50
Q

What are the clinical manifestations of a chronic pulmonary Blastomyces dermatitidis infection?

A
  • Fever, night sweats, fatigue, weight loss, cough, hemoptysis, and dyspnea
  • Chest x-ray with cavitary, nodular, fibrosis, mass like
51
Q

What is the Tx for a Blastomyces dermatitidis infection?

A
  • All patients should be treated
  • Itraconazole in mild disease
  • Amphotericin B in severe disease
52
Q

What kind of germ is Coccidioides immitis?

A
  • Dimorphic fungi
  • Inhaled arthroconidia enlarge and form spherules
  • Spherules undergo internal septation producing endospores
53
Q

Where is Coccidioides immitis endemic?

A

southwest deserts

54
Q

What are the clinical manifestations of a Coccidioides immitis infection?

A
  • Most asymptomatic
  • Pulmonary Infection
  • Symptoms develop 5-21 days after exposure
  • Fever, weight loss, fatigue, dry cough, and pleuritic chest pain
  • Arthralgias•Erythema nodosum
  • Pulmonary Nodule, cavitary
55
Q

What do you see on CXR of a Coccioides immitis infection?

A

•Chest x-ray with pulmonary infiltrates, hilar adenopathy, and peripneumonic effusion

56
Q

What people are at risk for getting a disseminated Coccidioides immitis infection? Where does it manifest?

A
  • Immunocompromised , e.g. AIDS
  • 3rd trimester pregnancy
  • Skin, joints, and bones
57
Q

What is the Tx for Coccidioides immitis infection?

A

itraconazole

Amphotericin B

58
Q

What kind of germ is Paracoccidioidomycosis brasiliensis?

A
  • Thermally dimorphic fungus
  • Morphology:
  • Thick-walled yeast cells that have multiple small circumferentially attached, narrow-based budding daughter yeast cells
  • Ship’s steering wheel
  • Lives in soil
  • Endemic to humid areas of Central and South America
59
Q

What population are Paracoccidioidomycosis brasiliensis infections most prevalent in?

A

•Most prevalent in middle-aged to elderly men

60
Q

When does an infection with Paracoccidioidomycosis brasiliensis develop? What forms can develop?

A
  • Paracoccidioidomycosis develops after inhalation of aerosolized conidia encountered in the environment
  • Acute-Subacute Paracoccidioidomycosis – less than 10%
  • RES with dissemination to the liver, spleen, lymph nodes, and bone marrow
61
Q

What are the clinical manifestations of chronic paracoccidioidomycosis? What do you see on CXR?

A
  • Progressive over many years
  • Most patients older men
  • Pulmonary involvement mimics tuberculosis
  • Ulcerative lesions in the anterior nares, oral cavity, and larynx that are slowly destructive
  • Chest x-ray with nodular, interstitial, and cavitary lesions in the middle or lower lung fields
62
Q

How do you Dx chronic paracoccidioidomycosis?

A

Growth in culture

63
Q

Where is Strongyloides stercoralis endemic?

A

warm climates worldwide

64
Q

How is Strongyloides stercoralis transmitted?

A

•Exposed skin comes in contact with free-living filiariform larvae living in contaminated soil. After skin penetration, larvae enter the afferent circulation and travel to the pulmonary vasculature, where they rupture into the alveolar spaces, ascend the respiratory tree, and are swallowed into the GI tract. Development into adult worms occurs in the upper part of the small intestine. Female worms begin laying eggs. Eggs hatch in the lumen of the small intestine. Rhabditiform larvae migrate to the colon and are passed in the feces.

65
Q

What are the pulmonary manifestations of a Strongyloies stercoralis infection?

A
  • Can be severe in immunocompromised
  • Resembles ARDS with acute onset of dyspnea, productive cough, and hemoptysis accompanied by fever, tachypnea, and hypoxemia
66
Q

What is the Tx for a Strongyloides stercoralis infection?

A

ivermectin

67
Q

What kind of microbe is Aspergillus? Where can it be found? How is it spread?

A
  • Aspergillus are ubiquitous organisms found in soil, decaying matter, and air.
  • Spore like conidia are aerosolized from the mold form of the organism. They reach tissue and form invasive hyphae.
  • Can be isolated from basements, crawl spaces, bedding, humidifiers, ventilation ducts, potted plants, dust, condiments, and marijuana
68
Q

What kind of infection does Aspergillus create? What are the symptoms?

A
  • Invasive Aspergillosis
  • Immunocompromised host
  • Fever
  • Pulmonary infiltrates
  • Nodules
  • Wedge-shaped densities resembling infarcts
  • Sinusitis
  • Extrapulmonary sites:
  • CNS abscesses, endophthalmitis, MI, GI, renal, osteomyelitis, endocarditis
69
Q

Who is at risk for Aspergillosis?

A

immunocompromised people

70
Q

How do you Dx invasive Aspergillosis?

A

•BAL, needle aspiration, thoracoscopic biopsy, or open lung biopsy

71
Q

How do you treat Aspergillosis?

A
  • Antifungal- Voriconazole or liposomal amphotericin B
  • Reversal of immunosuppression
  • Surgical resection of infected lesions
72
Q

What are the clinical manifestations of chronic pulmonary aspergillosis?

A
  • Chronic Pulmonary Aspergillosis
  • Aspergilloma
  • Ball in cavity
  • Debris in preformed cavity from TB, Histoplamosis, or fibrocystic sarcoidosis
73
Q

What is the treatment for chronic pulm aspergillosis?

A
  • Limited benefit with aspergilloma
  • Antifungal – itraconazole or voriconazole in chronic cavitary pulmonary aspergillosis
74
Q

What are the clinical manifestations of Allergic Bronchopulmonary Aspergillosis (ABPA)?

A

•Airway obstruction, fever, eosinophilia, positive sputum cultures, mucous plugs containing hyphae, brown flecks in sputum, transient infiltrates, proximal bronchiectasis, upper lobe contraction, elevated IgE.

75
Q

Who is at risk for ABPA?

A

People with a Hx of chronic asthma or CF (cystic fibrosis)

76
Q

How is ABPA Dx’ed?

A

•Eosinophilia in blood, sputum, and lung tissue

77
Q

How is allergic pulmonary aspergillosis Dx’ed?

A
  • Asthma
  • Immediate cutaneous reaction to A. fumigatus antigen
  • Serum IgE greater than 1000 ng/ml
  • A. fumigatus specific serum IgE levels
  • Precipitating serum antibodies to A. fumigatus
  • Central bronchiectasis
  • Peripheral eosinophilia
  • Pulmonary infiltrates
78
Q

How is allergic pulmonary aspergillosis treated?

A

corticosteroids and itraconazole

79
Q

What patient population does Cryptococcosis most commonly occur in?

A

HIV+ people

•Patients at highest risk are those with AIDS and CD4 counts less than 50.

80
Q

What is the most common clinical manifestation of Cryptococcosis? What other systems can be involved?

A

meningitis

  • Pulmonary and other organ involvement can occur
  • C. neoformans is neurotropic
81
Q

What kind of germ causes Cryptococcosis? Where does it reside?

A
  • Cryptococcus neoformans
  • Yeast
  • Environment and tissues
82
Q

What is the major virulence factor for Cryptococcosis/Cryptococcus neoformans?

A

polysaccharide capsule

83
Q

How is Cryptococcus neoformans transmitted?

A

•Inhaled from the environment and causes pulmonary infection initially. Most patient asymptomatic.

84
Q

What could happen if someone with an asymptomatic cryptococcus infection becomes immunocompromised?

A

•If the host becomes immunosuppressed the organism can reactivate and disseminate to other sites.

85
Q

What are the clinical manifestations of an infection with Cryptococcus neoformans in the CNS?

A
  • Meningoencephalitis
  • Headaches over several weeks
  • Nuchal rigidity
  • Lethargy
  • Personality changes
  • Confusion
  • Visual abnormalities
  • Nausea and vomiting
86
Q

What are the clinical manifestations for a pulmonary Cryptococcosis infection? What are the risk factors for this type of infection?

A
  • Pulmonary Infection
  • Risk factors include COPD, Corticosteroid use, and solid organ transplant
  • Fever, cough, and dyspnea
  • Treated with antifungals
87
Q

In addition to the pulmonary system and CNS, what other organs can be affected with a Cryptococcosis infection?

A

Skin, prostate, osteoarticular surfaces, breast, eye, and larynx

88
Q

How is a cryptococcosis infection Dx’ed?

A
  • Yeast is grown in culture from CSF, Blood, sputum, skin lesions, or other body fluids
  • India Ink stain – visualization of budding yeast with large capsule
  • Latex agglutination for Cryptococcal polysaccharide antigen
89
Q

How do you treat a CNS infection of Cryptococcosis? Is it different for different types of patients?

A
  • Non-AIDS Patients
  • Amphotericin B and flucytosine for 6 weeks
  • AIDS Patients
  • Amphotericin B and flucytosine for 2 weeks, followed by fluconazole 400 mg daily for 8 weeks, then suppressive therapy with fluconazole 200 mg daily
90
Q

What are the HACEK group organisms?

A
  • Haemophilus spp
  • Actinobacillus actinomycetemcomitans
  • Cardiobacterium hominis
  • Eikenella corrodens
  • Kingella spp
91
Q

What condition are HACEK organisms frequently associated with?

A
  • 5% of endocarditis cases
  • Common Cause of endocarditis in non-IV drug users
92
Q

Are the HACEK group organisms unusual or rare bacteria?

A

No - often normal flora

93
Q

How long does it take to Dx a HACEK infection?

A

•Difficult to diagnose- often takes 3 months

94
Q

What are the culture requirements for H. influenzae?

A

•Chocolate Agar with Factors V(NAD+) and X(Hematin)

95
Q

What are the culture requirements for N. meningitidis?

A

Thayer-Martin

96
Q

What are the culture requirements for B. pertussis?

A

Bordet-Gengou

97
Q

What are the culture requirements for C. diptheriae?

A

Loffler medium

98
Q

What are the culture requirements for M. Pneumoniae?

A

Eaton Agar- requires cholesterol

99
Q

What are the culture requirements for Legionella?

A

Charcoal Yeast Extract cysteine and iron

100
Q

What are the special stain requirements for Chlamydia?

A

Giemsa

101
Q

What are the special stain requirements for Cryptococcus?

A

India ink

102
Q

What are the special stain requirements for Pneumocystis?

A

Silver Stain

103
Q

What are the special stain requirements for Mycobacteria?

A

Ziehl-Neelsen

104
Q
A