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1. HDS Cardiology > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Malaria

Vector

A

Female anopheline mosquito

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2
Q

Malaria

Lifecycle

A
  • Sporozoites
    • Transmitted form
    • Innoculated from mosquito saliva
    • Rapidly cleared from blood in 15-30 minutes
  • Sporozoites ⇒ merozoites in hepatocytes
    • Asexual replication
    • Parasites contained within a Schizont
    • Non-pathogentic infection
  • Merozoites released from Schizont ⇒ RBC
  • Merozoite ⇒ trophozoites (ring stage) in RBC
    • Asexual replication inside RBC ⇒ release
      • Responsible for pathology
  • Merozoite ⇒ gametocyte
    • Sexual stage
    • Picked up by mosquitos that feeds
  • Gametocytes mature into gametes in mosquito gut
    • Fertilization ⇒ zygote ⇒ motile ookinete ⇒ penetrates gut ⇒ sporozoites ⇒ salivary glands
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3
Q

Plasmodium vivax

and

Plasmodium ovale

A
  • Tertian fever patterns
    • Sx every 3 days
  • Latent state
    • Long term persistance in the liver
    • Potential for reactivation
  • Prefers immature erythrocytes or reticulocytes
  • Lower parasitemia
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4
Q

Plasmodium malariae

A
  • Quartan fever pattern
    • Sx every 4 days
  • Frequently becomes synchronous in vivo
    • Periodic release of parasites with fever
  • Low parasitemia
  • Prefers senescent RBCs
  • No latent phase
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5
Q

P. falciparum

A
  • Asynchronous replication of blood-stage
    • Irregular fever pattern
  • Developmental period of 14 days
  • Characteristic crescent shape
  • Trophozoite and schizont forms occur in visceral capillaries ⇒ sequestration
  • Infects all RBCs ⇒ high parasitemia
  • Causes cerebral malaria
  • Reponsible for the most deaths
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6
Q

Malaria

Host Cell Invasion

A
  • Active process of the parasite
  • Interactions between parasite surface molecules and host receptors
  • Contents of apical organelles responsible
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7
Q

Malaria

Lifecycle Comparison

A
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8
Q

Malaria

Fever Generation

A
  • Usually paroxysmal except for P. falciparum
  • Coincides with parasite release from RBCs
  • Parasite products induce cytokine production
    • GPI anchors
    • Hemozoin
      • Malarial pigment produced from digestion of heme
  • Elevated TNF-α and IL-1
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9
Q

Malaria

Infectious Determinants

A
  • Host factors
    • Sickle cell trait & other hemoglobinopathies
      • Heterozygosity confirs resistance
    • Duffy blood group system
      • Duffy ⊖ cells resistant to P. vivax
  • Parasite factors
    • Multiplication rate
      • 1% parasitemia = 5x1010 in blood
    • Parasite “toxins”
    • Cytoadherence-dependent tissue distribution
      • Cerebral sequestration
      • Placental sequestration
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10
Q

Cytoadherence

A
  • Specific receptor-ligand interactions
  • Form knob-like structions on surface of RBCs ⇒ rosettes
    • Contain late stage trophozoites and schizonts (merozoites inside)
  • Knob-associated parasite proteins
    • PfEMP-1, rifin, stevor, clag
  • Host cell receptors on endothelium, placenta, and uninfected RBCs
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11
Q

Malaria

Diagnosis

A
  • History and clinical symptoms
  • Peripheral blood smears
    • Thick smears ⇒ parasite detection
    • Thin smears ⇒ species ID
    • P. falciparum ⇒ only see ring stages and banana shaped gametocytes in blood
      • Due to sequestration of mature stages
  • Detection of circulating parasite Ag or nucleic acid
    • HRP2 ⇒ secreted Ag
    • Lactate dehydrogenase
    • Dipstick and PCR
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12
Q

Uncomplicated Malaria

A
  • Often cyclic high fever and chills
  • Malaise
  • Myalgia
  • Dizziness
  • HA
  • Weakness
  • Nausea
  • Diarrhea
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13
Q

Recurrent Malarial Infections

A
  • Relapse from dormant liver stage ⇒ hypnozoites
    • P. vivax and P. ovale only
    • May occur within months to years after primary infection
  • Reinfection, multiple infections
    • Frequent w/ P. falciparum
    • Occurs w/ P. vivax
    • Immunity is region specific
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14
Q

Malaria

Recrudescence

A
  • Occurs esp. w/ P. falciparum
  • Due to:
    • Partially effective host immune response
    • Incomplete treatment and development of resistance
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15
Q

Severe Malaria

P. vivax

A
  • Severe anemia
  • Splenomegaly
  • Splenic rupture
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16
Q

Severe Malaria

P. malariae

A

Immune complex glomerulonephritis associated with persistent low level of parasitemia

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17
Q

Severe Malaria

P. falciparum

A
  • Splenomegaly
  • Lactic acidosis
  • Hypoglycemia
  • Severe anemia
  • Cerebral malaria
  • Acute renal failure
  • Pulmonary edema
  • Hyperparasitemia
  • Multi-organ failure
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18
Q

Cerebral Malaria

A
  • Severe complication of P. falciparum
  • Affects children 3-5 y/o
  • Parasitized RBC cytoadhere to endothelium of brain microvasculature
  • pRBCs form rosettes with uninfected RBCs
  • Pathogenesis
    • Ischemia/hypoxia
      • Occlude capillaries ⇒ impair flow of blood, oxygen, nutrients to brain
    • Inflammation
      • Inflammatory response ⇒ ↑ vascular permeability ⇒ tissue damage
  • Symptoms
    • Impaired consciousness
    • Cerebral dysfunction
    • Coma
    • Death ⇒ mortality rate 15-30% w/ tx
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19
Q

Severe Malarial

Anemia

A
  • Criteria
    • Hb < 7 g/dL or Hct < 20%
    • Presence of any malarial parasitemia
  • Almost always d/t P. falciparum
  • Mainly affects children < 1 y/o in sub-Saharan Africa
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20
Q

Malaria

Immunity

A
  • Acquired very slowly
  • Transient
    • Wanes rapidly if person leaves the area
  • Specific to region and strains
  • Likely involves both Ab and cell-mediated immunity but poorly understood
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21
Q

Malaria

Vaccines

A

Still in development

  • Sporozoites
    • Circumsporozoite surface protein target
      • Being tested
  • Erythrocytic stage
    • Major merozoite surface protein
    • Rhoptry proteins
    • Cytoadherence molecules
  • Gametocyte and zygotes
    • Transmission blocking immunity
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22
Q

Malaria

“Anti-disease” Immunity

A
  • People in endemic areas w/ persistent parasitemia may appear asymptomatic
  • Sterilizing immunity may not be possible
    • If possible, may be short lived and cause ↑ severity w/ subsequent infection
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23
Q

Hemoflagellates

A
  • Flagellated, insect-transmitted protozoa
  • Infects blood and tissues
  • Have kinetoplasts ⇒ specialized mitochondria at base of flagella
    • Contains maxicircle and minicircle DNA
      • Drug target and strain ID
  • Leishmania and Trypanosoma
    • Two major genera that cause human & domestic animal disease
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24
Q

Leishmania

Vector and Reservoirs

A

Vector ⇒ sandfly

(Phlebotomus and Lutzomyia)

Reservoirs ⇒ rodents, dogs, foxes, small mammals

Animal-vector-human cycle

Human-vector-human cycle

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25
Q

Leishmania

Lifecycle

A
  • Extracellular promastigotes in sandfly vector
    • Differentiate in salivary glands to metacyclic promastigotes ⇒ infectious form
  • Metacyclic promastigotes innoculated by sandfly during blood meal
    • Motile and resistant to complement
  • Metacyclic promastigotes invade macrophages
    • Differentiate into amastigote form
  • Amastigotes multiply within phagolysosome of Mφ
    • Cell lysis releases parasite for further spread
  • Amastigotes transferred to sandfly when infected host bitten
    • Differentiates back into promastigotes
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26
Q

Cutaneous Leishmaniasis

Organisms

A

Caused by 4 geographically specific species:

  • L. mexicana & L. braziliensis
    • South and central America
    • Can become visceral
  • L. major & L. tropica
    • Asia, Africa, Mediterreanan, Middle East, Russia
    • Typically remains cutaneous
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27
Q

Cutaneous Leishmaniasis

Pathogenesis

A
  • Red papule develops @ site of bite after 1 wk - 2 months
    • Secondary bacterial infections problematic
  • Becomes hard and crusted
  • Usually self-limiting but may persist for months to years
    • Resolution associated with protective immunity
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28
Q

Diffuse Cutaneous Leishmaniasis

A
  • Occurs with ineffective immune responses
    • Esp. cell-mediated
  • See massive, disseminated nodular skin lesions
    • Resembles leprosy
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29
Q

Mucocutaneous Leishmaniasis

A
  • Usually caused by L. braziliensis
    • Central and South America
  • Develops from cutaneous leishmaniasis
  • Spreads to mucosal surfaces
  • Destruction of mucous membranes and tissues
    • Edema
    • Secondary infections
    • Severe and disfiguring facial lesions
  • Intense inflammatory responses
    • May involve autoimmune component
30
Q

Visceral Leishmaniasis

Organisms

A

“Kala-azar or Black Fever”

  • Caused by 3 regionally specific species
    1. L. donovani
      • Asia, Africa, SE Asia
    2. L. chagasi
      • South and Central America
    3. L. infantum
      • Mediterranean basin
31
Q

Visceral Leishmaniasis

Pathogenesis

A

“Kala-Azar or Black Fever”

  • Incubation ⇒ weeks to years
    • No characteristic skin lesion
  • Parasites invade and proliferate in Mφ of liver and spleen
    • Gradual onset fever and anemia
    • Weight loss
    • Marked hepatosplenomegaly
    • Glomerulonephritis
  • May continue as a persistant chronic illness
    • Death in 1-2 years
  • May progress to fulminant deilitating disease
    • Death in weeks
  • HIV patients
    • Severe disease w/ unusual manifestations
    • Can invade CNS
  • Successful treatment for L. donovani can result in Post-Kala Azar Dermal Leishmaniasis (PKDL) in some pts
32
Q

Post-Kala Azar Dermal Leishmaniasis

(PKDL)

A
  • Follows after successful treatment of visceral leishmaniasis w/ L. donovani
  • Parasites persist in cutaneous nodules to varying degrees
33
Q

Leishmaniasis

Immunity

A

Different clinical pictures determined by subset of responding T-cells

  • Th1 response
    • IFN-𝛾 and Mφ activation
    • Strong cellular immunity
    • Limited course of disease
  • Th2 response
    • Strong Ab response
    • Ineffective against intracellular parasites
    • Disease progression
  • Believed that parasites persist for life ⇒ reactivation
34
Q

Leishmaniasis

Diagnosis

A
  • Microscopic examination of specimen
    • Cutaneous/mucocutaneous ⇒ skin ulcers
    • Visceral ⇒ tissue biopsy or bone marrow aspirates
    • Demonstrate amastigotes in macrophages ⇒ Leishman-Donovan bodies
  • Culture of specimen
  • Leishmanin skin test
    • DTH serologic testing
    • Not for disseminated disease
    • Limited use in highly endemic areas
35
Q

Leishmaniasis

Treatment

A
  • Ulcer management
  • Prevention of secondary infections
  • Severe localized or disseminated disease
    • Pentavalent antimonials
      • Heavy metal drugs that intefere w/ sulfhydryl groups
    • Pentamidine
      • Interferes with DNA
    • Amphotericin B
      • Binds sterols in parasite membrane
  • High toxicity of drugs, high cost, treatment failure
36
Q

Trypanosoma

Life Cycle

A
  • Epimastigote in insect vector
    • Flagella w/ partial undulating membrane
  • Trypomastigote in mammalian host
    • Flagella w/ full undulating membrane
  • Amastigote found intracellularly in infected mammalian host
    • Not all species
37
Q

African Trypanosomiasis

A

“African Sleeping Sickness”

  • Caused by Trypanosoma brucei species
  • Causes disease in human and lifestock
    • Humans ⇒ sleeping sickness
    • Cattle ⇒ Nagana
38
Q

Trypanosoma brucei

Vector

A

Tsetse flies

39
Q

Trypanosoma brucei

Species

A

3 subspecies of Trypanosoma brucei

  • T. b. gambiense ⇒ more chronic
    • West and Central Africa
    • Human disease
    • Domestic pigs reservoir
  • T. b. rhodesiense ⇒ more acute
    • East Africa
    • Human disease in hunters, travelers
    • Cattle and sheep reservoirs
40
Q

Trypanosoma brucei

Lifecycle

A
  • Metacyclic trypomastigotes injected by Tsetse fly
  • Transform into bloodstream trypomastigotes remain extracellular in the blood, lymph, and spinal fluid
    • Divide by binary fission
  • No intracellular amastigote state present
41
Q

African Trypanosomiasis

Pathogenesis

A

“African Sleeping Sickness”

  • Chancre often develops @ site of bite
  • Parasites disseminate into through blood stream and lymphatics 2-3 weeks later
    • Fever
    • Myalgias
    • Arthralgia
    • Lymph node enlargement
      • Swelling of posterior cervical lymph nodes ⇒ Winterbottom’s sign
  • Chronic disease develops over several weeks of parasitemia
    • Body makes neutralizing Ab
    • Parasites change surface Ag
  • Cycles of blood parasitemia and cyclic fever pattern
    • Lymphadenopathy, HA, and neurological sx
    • Also kidney damage and myocarditis with T. b. rhodesiense
  • Localization of parasites in small blood vessels of heart and CNS
  • ‘Sleepining sickness’ starts after CNS invasion
    • Meningoencephalitis
    • Lethargy, tremors, coma
  • Death from CNS damage, heart failure, or secondary infections
    • Usually within 9-12 months if untreated
42
Q

African Trypanosomiasis

Immune Response

A

Effective humoral immunity.

Periodic variation of parasite’s major surface Ag ⇒ chronic infection and fluctuating parasitemia

Results from DNA rearragements of “silent” gene copies to “expression-linked” locus

43
Q

African Trypanosomiasis

Diagnosis and Treatment

A
  • Diagnosis
    • Microscopic examination of blood, CSF, or lymph node aspirates
    • Demonstration of trypomastigotes
  • Treatment
    • Acute blood and lymphatic stages
      • Suramin
      • Pentamidine
    • CNS-penetrating neurologic stage
      • DFMO (Difluoromethyl ornithine)
      • Melarsoprol
        • Very toxic, up to 5% die from tx
  • Prevention
    • Tsetse fly vector control
    • Elimination of animal reservoirs
    • Largely unsuccessful
44
Q

American Trypanosomiasis

A

“Chagas’ Disease”

  • Caused by Trypanosoma cruzi
  • Found in central and south America
45
Q

Trypanosoma cruzi

Transmission

A
  • 1° transmission
    • Vector ⇒ Reduviid bugs
      • “Kissing bugs”
      • Triatoma infestans
    • Reservoirs
      • Domestic dogs and cats
      • Wild animals like rodents, armadillos, raccoons, opossums, etcs
  • 2° transmission
    • Blood transfusions
46
Q

Trypanosoma cruzi

Lifecycle

A
  • Metacyclic trypomastigotes present in feces of reduviid bugs
    • Bugs often bite near the eyes or lips
    • Parasites released in bug feces
    • Rubbed into bite or conjunctiva
  • Blood trypomastigotes can infect nearly every cell type
    • Prefers macrophages, cardiac muscle cells, and glial cells
    • Enters via receptor-mediated endocytosis
  • Escape from phagosome into cytosol
    • TcTox, Cholesterol-dependent cytolysin
  • Differentiate into amastigotes in host cell cytoplasm and divide
  • When cytoplasm full, revert back into flagellated trypomastigotes
    • Infect new host cells upon release
  • Asymptomatic infection or acute febrile disease
47
Q

Acute Chagas’ Disease

A

Primarily in children:

  • Chagoma develops at site of bite
    • Erythematous indurated nodule
    • Infection via conjunctiva ⇒ unilateral chagoma of the eye ⇒ Romana’s sign
  • Acute infection progresses to
    • Fever
    • Myalgias
    • Fatigue
    • Hepatosplenomegaly
    • Lymphadenopathy
  • The patient may
    1. Die from infection within several weeks
    2. Recover completely
    3. Enter chronic phase
48
Q

Chronic Chagas’ Disease

A

Parasites proliferate and invade the heart, liver, spleen, and lymph nodes.

May develop years after acute infection.

  • Hepatosplenomegaly
  • Myocarditis and cardiomyopathy
  • Megacolon / megaesophagus
    • Due to destruction of ANS nerves
  • Progressive destruction of NMJ
  • CNS involvement
    • Granulomas
    • Cyst formation
    • Meningoencephalitis
49
Q

African Trypanosomiasis

Immunity

A
  • Activation of macrophages
  • CD8+ T cell mediated lysis of infected cells
  • Ab opsonization and lysis of extracellular trypomastigotes by complement
  • Chronic disease may involve an autoimmune component
  • No vaccines available
50
Q

African Trypanosomiasis

Diagnosis and Treatment

A
  • Diagnosis
    • Acute disease
      • Microscopic examination of blood or biopsy
    • Chronic disease
      • Serological tests
        • IFA, ELISA, complement fixation
      • Clinical signs
    • Xenodiagnosis in endemic areas
      • Uninfected reduviid bugs allowed to feed on pt and parasites detected in vector
  • Treatment ⇒ highest efficacy during acute infection
    • Nifurtimox
    • Benznidazole
    • Allopurinol
51
Q

Streptococcus pyogenes

Characteristics

A
  • Lancefield group A strep ⇒ GAS
  • Gram ⊕ cocci in chains
  • Catalase ⊖
  • β-hemolytic
  • Bacitracin sensitive
52
Q

GAS

Virulence Factors

A
  1. M protein + lipotechoic acid (LTA) ⇒ pili
    • M protein ⇒ adhesin for attachment to keratinocytes
      • Antiphagocytic and anti-complement
      • Immunologically cross-reactive to human cardiac muscle tissue ⇒ RHD
  2. Capsule
    • Anti-phagocytic
    • Made of hyaluronic acid ⇒ non-immunogenic
  3. Streptococcal Pyrogenic toxin (SPE)
    or erythrogenic toxin
    • 3 forms ⇒ SPE A, B, C
    • Direct toxic damage to skin
    • Produce DTH response ⇒ rash in Scarlet fever
    • Superantigens ⇒ TNF and IL-1 production
    • Lysogeny/lysogenic conversion for SPE A and C
      • Transmitted by bacteriophage
  4. Streptolysin O and Streptolysin S
    • Hemolytic and cytotoxic to WBCs
  5. Streptodornase (DNAse), streptokinase, hyaluronidase
    • Faciliate invasion of tissues and dissemination
53
Q

S. pyogenes

Pathologies

A
  • Primary infections
    ⇒ acute pyogenic infections of any tissue
    • Pharyngitis or tonsillitis
    • Scarlet fever
    • Impetigo
    • Otitis media, sinusitis, mastoiditis, bacteremia, PNA
  • Post-streptococcal sequelae
    ⇒ non-suppurative, non-infectious sequelae following primary infection
    • Acute Rheumatic Fever (ARF) / Rheumatic Heart Disease (RHD)
    • Post-streptococcal Acute Glomerulonephritis (PSAGN)
54
Q

Streptococcal Pharyngitis

Epidemiology and Transmission

A
  • Most common cause of bacterial pharyngitis ⇒ 12-30%
  • Winter and early spring
  • Greatest incidence in 5-15 y/o
  • Exogenous transmission by respiratory droplets
  • Asymptomatic nasal and pharyngeal carriers
  • Children can be chronically infected after treatment
55
Q

Strep Pharyngitis

Clinical Manifestations

A
  • Sore throat w/ white exudates
  • Tonsils enlarged and erythematous
  • Anterior cervical lymphadenopathy
  • No cough
  • Fever
  • Malaise
  • HA
56
Q

Scarlet Fever

A

Can accompany pharyngitis or impetigo.

  • Generalized punctate erythematous rash ⇒ “sandpaper rash”
    • Caused by pyrogenic toxin (SPE)
      • Carried by tox ⊕ lysogenic bacteriophage
  • Strawberry tongue
  • Fever
57
Q

Acute Rheumatic Fever (ARF) / Rheumatic Heart Disease (RHD)

Pathogenesis

A
  • Follows respiratory but not skin infections
    • Typically 1-5 wks s/p strep pharyngitis
  • Type II hypersensitivity
  • Cross-reactivity of Ab against M-protein
    • Certain serotypes considered Rheumatogenic
  • Targets heart, joint, blood vessels, and nervous tissue
58
Q

ARF

Epidemiology

A
  • 0.5-3% incidence in US
    • Much higher in developing countries
  • May follow severe or asymptomatic infection
  • Peak age 6-20 y/o
59
Q

ARF/RHD

Clinical Manifestation

A
  • Carditis
    • Inflammation of myocardium or endocardium
    • Can see polycarditis w/ all 3 layers
    • Mitral and/or aortic valve damage
  • Polyarthritis
  • Rash (erythema marginatum)
  • Chorea
  • Subcutaneous nodules
60
Q

Post-Streptococcal Acute Glomerulonephritis

(PSAGN)

A
  • Follows cutaneous or respiratory infection
    • Typically 1-2 wks s/p strep pharyngitis
  • Type III Hypersensitivity
    • Strep Ag-Ab complexes deposition on glomerular basement membrane and excessive inflammatory response
  • Clinical features
    • Facial edema
    • Dark urine / hematuria
    • Proteinuria
    • HTN
61
Q

Acute Strep Infection

Diagnosis

A

Pharyngitis and Scarlet Fever

  • Rapid Ag Detection
    • Performed in office
    • High specificity ⇒ ~100%
    • Low sensitivity ⇒ 70-90%
      • Need to culture
  • Culture from swab/blood samples
    • Gram ⊕ cocci in chains
    • Grown on blood agar ⇒ β-hemolytic
    • Catalase ⊖
      • Staph ⇒ catalase ⊕
    • Bacitracin sensitive and CAMP ⊖
      • Group B strep ⇒ resistant and CAMP ⊕
62
Q

Strep

Serologic Tests

A

RF and PSAGN

  • Ab to 5 group A strep Ag
    • Streptolysin O (ASO) ⇒ most widely used
    • DNAse B
    • Streptokinase
    • Hyaluronidase
    • NADase
  • Streptozyme test
    • Combo test for all 5 Ab’s
    • Based on agglutination of Ag-coated RBCs by Ab in pts serum
  • Used for dx of RF/PSAGN and monitoring progress
63
Q

S. pyogenes

Treatment

A
  • Penicillin, ampicillin, or amoxicillin x 10 days
  • Erythromycin for pts w/ PCN allergies
  • No documented cases of resistance
64
Q

Post-strep Sequelae

Prevention

A
  • Starting abx within 10 days of onset for strep pharyngitis protects against rheumatic fever
    • Complete course must be taken
  • RHD pts need anti-microbial prophylaxis
    • Min. 10 yrs
    • Recurrent strep infections can worsen disease
  • Treatment does not protect against glomerulonephritis
65
Q

Staphylococcus aureus

A
  • Characteristics
    • Gram ⊕ cocci in clusters
    • Catalase ⊕
      • Differentiates Staph from Strep
    • Coagulase ⊕
      • Differentiates S. aureus from other Staph
    • β-hemolytic
  • Most Staph infections are endogenously acquired
    • Normal flora of skin and nares in 30-40%
  • > 90% resistant to PCN
    • Penicillinase
    • Alterations to PBP
66
Q

Staphylococcus epidermidis

A
  • Characteristics
    • Gram ⊕ cocci in clusters
    • Catalase ⊕
    • Coagulase ⊖
    • 𝛾-hemolytic, white colonies (non-hemolytic)
  • Normal flora of the skin, nose, throat
  • Most common cause of prosthetic valve endocarditis
  • Ass. w/ infections of cardio and ortho prostheses, CSF shunts, vascular grafts, catheters
  • Makes HMW polysacc. slime ⇒ adherence to FB surfaces
  • Most strains resistant to PCN
  • Many resistant to β-lactamase-resistant PCN
67
Q

Streptococcus

A
  • Gram ⊕ cocci in chains
  • Catalase ⊖
  • Lancefield’s grouping A-U based on C carbohydrate
  • Non-groupable strep
    • Viridans group
    • Strep. pneumoniae
    • Peptostreptococcus ⇒ anaerobic
68
Q

Viridans Streptococci

Organisms

A
  1. S. mutans
  2. S. mitis
  3. S. salivarius
  4. S. sanguis
69
Q

Viridans Streptococci

Characteristics

A
  • Catalase ⊖
  • α-hemolytic
  • Optochin-resistant
  • Normal flora of mouth, skin, nasopharynx, GU tract, and GI tract
  • Low virulence
  • Clinical diseases include:
    • Dental caries ⇒ S. mutans
    • Infective endocarditis
      • Most frequent cause of NV-SBE
      • Usually 2/2 damaged heart tissue
      • Often after dental procedures
      • S. sanguis most common
  • Usually sensitive to PCN
70
Q

Nutritionally Variant Strep

A
  • Can cause culture negative endocarditis
  • Do not grow on standard lab media
    • Need L-cysteine and Vit B6
  • Generally belong to viridans strep
    • S. mitis common
71
Q

HACEK Organisms

A
  • Includes:
    • Haemophilus
    • Aggregatibacter (Actinobacillus)
    • Cardiobacterium
    • Eikenella
    • Kingella
  • Fastidious, slow growing, gram ⊖ organisms
  • Normal flora
  • Possible cause of culture negative endocarditis
72
Q

Enterococcus

A
  • Previously considered group D strep
  • Characteristics
    • Gram ⊕ cocci in short chains, pairs, singles
    • Catalase ⊖
    • Grow in 6.5% NaCl at 45°C
      • Remaining group D strep cannot
    • Most are alpha or gamma hemolytic
    • Few are beta hemolytic
    • Bile-esculin ⊕
  • Normal flora of skin, URT, GI, GU
  • E. faecalis ⇒ most important clinically
    • Opportunistic pathogen
      • UTI
      • Infective endocarditis
      • Meningitis
      • Bacteremia and septicemia
      • Intraabdominal and pelvic infecitons
  • Ampicillin or penicillin + aminoglycoside indicated
  • Vancomycin for resistant strains
  • VRE strains exist

1. HDS Cardiology (7 decks)

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