Microbiology Flashcards
(72 cards)
1
Q
Malaria
Vector
A
Female anopheline mosquito
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
- Asexual replication inside RBC ⇒ release
-
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
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
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
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
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
7
Q
Malaria
Lifecycle Comparison
A
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
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
-
Sickle cell trait & other hemoglobinopathies
-
Parasite factors
- Multiplication rate
- 1% parasitemia = 5x1010 in blood
- Parasite “toxins”
-
Cytoadherence-dependent tissue distribution
- Cerebral sequestration
- Placental sequestration
- Multiplication rate
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
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
12
Q
Uncomplicated Malaria
A
- Often cyclic high fever and chills
- Malaise
- Myalgia
- Dizziness
- HA
- Weakness
- Nausea
- Diarrhea
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
14
Q
Malaria
Recrudescence
A
- Occurs esp. w/ P. falciparum
- Due to:
- Partially effective host immune response
- Incomplete treatment and development of resistance
15
Q
Severe Malaria
P. vivax
A
- Severe anemia
- Splenomegaly
- Splenic rupture
16
Q
Severe Malaria
P. malariae
A
Immune complex glomerulonephritis associated with persistent low level of parasitemia
17
Q
Severe Malaria
P. falciparum
A
- Splenomegaly
- Lactic acidosis
- Hypoglycemia
- Severe anemia
- Cerebral malaria
- Acute renal failure
- Pulmonary edema
- Hyperparasitemia
- Multi-organ failure
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
-
Ischemia/hypoxia
-
Symptoms
- Impaired consciousness
- Cerebral dysfunction
- Coma
- Death ⇒ mortality rate 15-30% w/ tx
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
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
21
Q
Malaria
Vaccines
A
Still in development
- Sporozoites
- Circumsporozoite surface protein target
- Being tested
- Circumsporozoite surface protein target
- Erythrocytic stage
- Major merozoite surface protein
- Rhoptry proteins
- Cytoadherence molecules
- Gametocyte and zygotes
- Transmission blocking immunity
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
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
-
Contains maxicircle and minicircle DNA
-
Leishmania and Trypanosoma
- Two major genera that cause human & domestic animal disease
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
25
Leishmania
Lifecycle
* 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**
26
Cutaneous Leishmaniasis
Organisms
_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
27
Cutaneous Leishmaniasis
Pathogenesis
* **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
28
Diffuse Cutaneous Leishmaniasis
* Occurs with **ineffective immune responses**
* Esp. cell-mediated
* See **massive, disseminated nodular skin lesions**
* Resembles leprosy
29
Mucocutaneous Leishmaniasis
* 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
Visceral Leishmaniasis
Organisms
"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
Visceral Leishmaniasis
Pathogenesis
"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
Post-Kala Azar Dermal Leishmaniasis
| (PKDL)
* Follows after successful treatment of visceral leishmaniasis w/ L. donovani
* Parasites persist in cutaneous nodules to varying degrees
33
Leishmaniasis
Immunity
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
Leishmaniasis
Diagnosis
* **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
Leishmaniasis
Treatment
* **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
Trypanosoma
Life Cycle
* **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
African Trypanosomiasis
"African Sleeping Sickness"
* **Caused by Trypanosoma brucei species**
* Causes disease in human and lifestock
* Humans ⇒ sleeping sickness
* Cattle ⇒ Nagana
38
Trypanosoma brucei
Vector
Tsetse flies
39
Trypanosoma brucei
Species
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
Trypanosoma brucei
Lifecycle
* **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
African Trypanosomiasis
Pathogenesis
"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
African Trypanosomiasis
Immune Response
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
African Trypanosomiasis
Diagnosis and Treatment
* _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
American Trypanosomiasis
"Chagas' Disease"
* **Caused by Trypanosoma cruzi**
* Found in central and south America
45
Trypanosoma cruzi
Transmission
* 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
Trypanosoma cruzi
Lifecycle
* **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
Acute Chagas' Disease
**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
Chronic Chagas' Disease
**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
African Trypanosomiasis
Immunity
* 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
African Trypanosomiasis
Diagnosis and Treatment
* _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
Streptococcus pyogenes
Characteristics
* Lancefield group A strep ⇒ **GAS**
* **Gram ⊕ cocci** in chains
* **Catalase ⊖**
* **β-hemolytic**
* **Bacitracin sensitive**
52
GAS
Virulence Factors
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
S. pyogenes
Pathologies
* **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
Streptococcal Pharyngitis
Epidemiology and Transmission
* **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
Strep Pharyngitis
Clinical Manifestations
* **Sore throat w/ white exudates**
* Tonsils enlarged and erythematous
* Anterior cervical lymphadenopathy
* No cough
* Fever
* Malaise
* HA
56
Scarlet Fever
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
Acute Rheumatic Fever (ARF) / Rheumatic Heart Disease (RHD)
Pathogenesis
* **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
ARF
Epidemiology
* 0.5-3% incidence in US
* Much higher in developing countries
* May follow severe or asymptomatic infection
* Peak age 6-20 y/o
59
ARF/RHD
Clinical Manifestation
* **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
Post-Streptococcal Acute Glomerulonephritis
(PSAGN)
* **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
Acute Strep Infection
Diagnosis
_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
Strep
Serologic Tests
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
S. pyogenes
Treatment
* **Penicillin, ampicillin, or amoxicillin x 10 days**
* **Erythromycin** for pts w/ PCN allergies
* No documented cases of resistance
64
Post-strep Sequelae
Prevention
* **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
Staphylococcus aureus
* 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
Staphylococcus epidermidis
* 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
Streptococcus
* Gram ⊕ cocci in chains
* Catalase ⊖
* Lancefield's grouping A-U based on C carbohydrate
* Non-groupable strep
* Viridans group
* Strep. pneumoniae
* Peptostreptococcus ⇒ anaerobic
68
Viridans Streptococci
Organisms
1. S. mutans
2. S. mitis
3. S. salivarius
4. S. sanguis
69
Viridans Streptococci
Characteristics
* **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
Nutritionally Variant Strep
* 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
HACEK Organisms
* Includes:
* **Haemophilus**
* **Aggregatibacter (Actinobacillus)**
* **Cardiobacterium**
* **Eikenella**
* **Kingella**
* Fastidious, slow growing, **gram ⊖ organisms**
* Normal flora
* Possible cause of culture negative endocarditis
72
Enterococcus
* 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
