Bacteremia Flashcards
Spontaneous bacteremia
common event (flossing, brushing teeth) that creates small lacerations allowing small amt of bacteria to enter the blood (minutes)
Transient bacteremia
trauma to a heavily colonized mucosal surface resulting in bacteria entering into the blood (hours)
Intermittent/Recurrent bacteremia
foci of infection (staph abscess) causing there to be bacteria in the blood occasionally
Continuous bacteremia:
certain diseases cause there to be bacteria in the blood continuously
Causes of Continuous bacteremia:
• Infective endocarditis, typhoid fever, anthrax, rickettsia, pyelonephritis, bacterial meningitis
Organs that clear bacteria from blood
liver & spleen
_______________ kill bacteria in the liver and spleen
Kupffer cells + PMNs
Asplenics are particularly susceptible
bacteremia, particularly those w/ capsules
Agents of bacteremia
CoNS, S. aureus, Enterococcus, GNRs, Strep, Candida
Risks for bacteremia
HA-bacteremia: CVC, catheters (Staph, E.coli)
CA-bacteremia:acute pyelonephritis
Catheter associated bacteremia agents
E.coli, GNR
CVC associated bacteremia agents
Staph
Common cause of bacteremia in children < 2
S. agalactiae, E. coli, K. pneumo
Common cause of bacteremia in elderly
GNR
Pathogenesis of catheter associated bacteremia
spread from skin to catheter, biofilm formation
S/S Bacteremia
Sepsis, severe sepsis, septic shock
Diagnosis of Bacteremia
Blood specimen collected 2-3 separate times over a 24hr period , >15m apart, before Abx Tx, before/during fever spike
Native Valve Endocarditis
most common, occurs in pts w/o hx of IVDU or prosthetic valve
Native Valve Endocarditis valves affected
mitral, aortic
Risks for Native Valve Endocarditis
mitral valve prolapse, congenital or acquired heart defects, rheumatic heart disease
Pathogenesis of Native Valve Endocarditis
turbulent BF -> deposition of fibrin/proteins/etc -> contamination of damaged heart valve secondary to bacteremia
Agents of Native Valve Endocarditis
Strep —> CoNS, S. aureus, GNR, S. pneumo, GAS
Prosthetic Valve Endocarditis
occurs in pts w/ prosthetic valves
Early Prosthetic Valve Endocarditis d/t
Contamination of valve during surgery
Agents of Early Prosthetic Valve Endocarditis
Strep —> CoNS, S. aureus, GNR, S. pneumo, GAS
Late Prosthetic Valve Endocarditis d/t
secondary to bacteremia
IVDU Endocarditis
least common, acute disease d/t contamination of the valve secondary to bacteremia
Most common valve affected by IVDU Endocarditis
tricuspid
Agents of IVDU Endocarditis
CoNS, S. aureus, Enterococci, S. pneumo, GAS, polymicrobic
Pathogenesis of IE
deposition of fibrin & platelet aggregation -> NBT -> bacteremia & secondary infection -> vegetation/biofilm -> large/small emboli
Immunopathology d/t IE
Hypergammaglobulinemia
Type III HSN reaction -> acute vasculitis & glomerulonephritis
Subacute IE Sx
low virulent; slow progression, immune pathology d/t Type III HSN, vasculitis, glomerulonephritis;
Fever, wt loss, anemia, leukocytosis, splenomegaly, mild heart murmur, Roth’s spots, CHF, emboli + Peripheral STIGMATA
Skin manifestations/Peripheral Stigmata of Subacute IE
petechiae on mucosa (conjunctiva), Janeway’s Lesions, Osler’s Nodes, Splinter hemorrhages, clubbing
Janeway’s Lesions
painless, petechial lesion on palms and soles
Osler’s Nodes
painful, petechial lesions on fingers & toes
Acute IE Sx
high virulent; rapid septic emboli -> ischemic event: Stroke, MI, Liver or Kidney Failure; Fever, significant heart murmur, w/o other S/S of immunopathology
Diagnosis of IE
transesophageal ECHO, blood specimen (2-3X), MIC/MBC/Cidal, Culture
Failure to culture for IE d/t HACEK
- Haemophilus
- Aggregaitbacter
- Cardiobacterium hominis
- Eikenella corrodens
- Kingella kingae
Treatment of IE
10X MBC
Prevention of IE
abx prophylaxis for procedures w/ risk of bacteremia (tooth extraction, cardiac, GI); Amoxicillin 30m before, 2hrs after
Old World visceral leishmaniasis causative agents
L. donovani donovani, L. donovani infantum, L. donovani archibaldi
New World visceral leishmaniasis causative agents
L. donovani chagasi
L. donovani characteristics
Small, round protozoan parasite of the macrophage family; obligate intracellular
Promastigote form
carried by sandflies & infects humans/reservoirs
Amastigote form
carried by humans/reservoirs & infects sandflies
Life Cycle of L. donovani
sandfly bites a human -> promastogotes are released & engulfed by macrophages -> divide, fill cytoplasm, cause macrophage cell lysis -> release of amastigotes -> taken up by new macrophages
L. donovani has a Predilection for
mononuclear cell populations, spleen, liver, bone marrow -> histiocyte and macrophage destruction
Vector of L. donovani in the Old World
Sandflies (Phlebotomus)
L. donovani infection in US
immigrants, travelers, troops
L. donovani is common
in India, Bangladesh, Middle East, Mediterranean, Africa, C. & S. America
Vector of L. donovani in the New World
Lutzomyia spp
Immune Response to L. donovani
CMI: Th1 cells produce IFN-gamma which activates macrophages to restrict intracellular growth
L. donovani has what affect on the immune system
amastigotes drive the immune response towards Th2 (production of Ab) & away from Th1, resulting in suppressed CMI & high levels of circulating Ig. Abs are ineffective
Visceral Leishmaniasis incubation period
~3-6mo
Manifestations of Visceral Leishmaniasis: Insidious
Insidious onset: hepatosplenomegaly, weight loss, fever, malaise, LAD, scaly skin/ashen appearance, cachexia
Manifestations of Visceral Leishmaniasis: Abrupt
Dromedary fever (intermittent high fever w/ 2X/d spikes, weak & feverish, but does not feel very ill!!! Generalized LAD and HSM eventually develop; intermittent fever continues for wks/mos while pt becomes emaciated & weak; Uncontrolled hemorrhage & anemia
Post-Kala-azar Dermal Leishmaniasis:
1-2yrs later; multiple erythematous macules -> large, non-tender nodules may appear on the face & upper body; Lesions are filled w/ Leishmaniae-infected histiocytes
Mortality of Visceral Leishmaniasis is d/t
secondary infection
Diagnosis: Labs w/ Visceral Leishmaniasis
Granulocytopenia, anemia, elevated gamma-globulins
Visceral Leishmaniasis Microscopy
Biopsy of bone marrow + Giemsa Stain - intracellular amastigotes in macrophages is a confirming diagnosis
Leishman Intradermal Skin Test
used retrospectively (post-infection); Negative during active infection d/t CMI anergy
Treatment for Visceral Leishmaniasis
Pentavalent antimony, Sodium Stibogluconat
Treatment for relapsed Visceral Leishmaniasis
Pentamidine isoethionate or Amphotericin B
Cutaneous Leishmaniasis Old World Agents
L. tropica, L. major, L. aethiopica
Cutaneous Leishmaniasis New World Agents
L. mexicana, L. amazonenesis, L. peruviana
Mucocutaneous Leishmaniasis Agents
L. braziliensis, L. guyanensis, L. panamensis
Incubation period of Cutaneous Leishmaniasis
1-3mo
Cutaneous Leishmaniasis Sx
1 dry ulcer or multiple wet ulcers; at site of infection, erythematous papule that gradually increases in size & evolves into a painless, non-pruritic plaque or ulcer, no systemic S/S
Leichmaniasis Recidivans – Hyperergic Variant:
Tubercles or nodules appearing over/around scars of healed ulcers; DTH response
Diffuse Cutaneous Leishmaniasis – Anergic Variant
anergic & the organisms disseminate throughout the skin; Th2 response
Mucocutaneous Leishmaniasis Sx
initial lesion is similar to the cutaneous form, but metastatic spread occurs to the nasal or oral mucosa (during or mos/yrs after primary lesion has healed)
Mucocutaneous Leishmaniasis Secondary lesions on mucosa
have intense mononuclear infiltrate w/ few/no parasites; Inflammatory cells release proteases -> erodes oronasal or oropharyngeal mucosa -> ulceration of the ST and cartilage -> loss of lips, soft part of nose, nasal septum, and soft palate
Trypansoma cruzi
Obligate intracellular protozoan hemoflagellate w/ a “C” or “U” shaped appearance
Chagas’ Disease locations
C. & S. America are infected
Trypansoma cruzi found in human peripheral blood
Trypomastigote form
Trypansoma cruzi Life Cycle
Metacyclin form invades cells locally -> transform to amastigote forms -> multiply & fill cytoplasm -> differentiate to trypomastigotes
Trypomastigotes lyse the host cell -> hematogenous spread to distant site
Trypansoma cruzi immune response
CMI; invades SM and evades CMI
Acute Chagas
Mild, localized inflammatory reaction at inoculation site; followed by parasitemia (fever, LAD, HSM, malaise) lasting 4-6wks
Chagoma Sign
erythematous subcutaneous nodule may form at inoculation site
Romana Sign
edema of the conjunctiva or eyelids if inoculation is via the oral, nasal, or ocular mucosa
Indeterminant Phase of Chagas
vague GI or Cardiac Sx, life-long persistent low-grade parasitemia
Chronic Chagas
occur years/decades after an acute infection d/t chronic inflammatory responses (Th1-mediated) to persisting antigens of organisms, resulting in fibrosis
Sx of Chronic Chagas
biventricular enlargement w/ thinning of the ventricular walls, conduction system defect, dysarrhythmias, cardiomyopathy, thromboembolism; Megacolon or Megaesophagus may develop: dysphagia, regurgitation, aspiration, constipation
Acute Chagas Diagnosis
peripheral blood smears: motile parasites on direct examination “C” shaped
Chronic Chagas Diagnosis
Serology to detect specific Abs
Treatment of Chagas
Nifurtimox & Benzidiazole (50% efficacy)
Acute chagas, which organs are heavily parasitized
heart & GI
West Africa Sleeping Sickness Agent
T. brucei gambiense
T. brucei vector
Tetse Fly
T. brucei evades immune system by
antigenic variation of VSG intracellularly
Primary Lesion of African Trypanosomiasis
chancre may form at bite site (painful, well-circumscribed, rubbery, red lesion, 2-5cm)
Hemolymphatic Stage of African Trypanosomiasis
invade the lymphatics resulting in febrile attacks lasting 3-7d, followed by asymptomatic interval
Hemolymphatic Stage of African Trypanosomiasis Sx
fever, malaise, HA, arthralgia, LAD, rash
Winterbottom’s Sign
Posterior cervical lymph node enlargement w/ African Trypanosomiasis Hemolymphatic Stage
Meningoencepphalitic Stage of African Trypanosomiasis Sx
delayed & prolonged pain sensation (Kerandel’s Sign), increasing loss of energy -> unresponsive, loss of motor control, difficult to arouse
Kerandel’s Sign
delayed & prolonged pain sensation; Meningoencepphalitic Stage of African Trypanosomiasis
T. brucei Diagnosis
“S” shaped protozoan on wet mount
Meningoencephalitic stage diagnosis
elevation of WBCs (>5) in CSF, elevated protein & intracranial pressure, + Mott Cells
Mott Cells
large eosinophilic plasma cells containing IgM – is an uncommon, but characteristic finding in CSF
Treatment of African Trypanosomiasis w/o CNS involvement
Suramin or Pentamidine
Treatment of African Trypanosomiasis w CNS involvement
Malarsoprol or Eflornithine
Toxoplasma gondii
protozoan, obligate intracellular, 2 life forms in humans
Tachyzoite
invasive, rapidly proliferating trophozoite found in any nucleated cell, predilection for mononuclear phagocytes
Bradyzoite
pseudocysts found in muscle and brain, dormant/slow replication; Host’s CMI response forms tissue pseudocysts
Life Cycle of T. gondii
intermediate host ingests either a mature oocyst or pseudocyst -> sporozoites (from oocyst) or trophozoites (from pseudocyst) invade the GIT epithelium
-> picked up by macrophages -> tachyzoites multiply rapidly -> lyses cell & spread hematogenously to all tissues -> small necrotic foci lead to CMI response -> pseudocyst
Leading cause of death d/t food-borne illness in the US
T. gondii
2nd leading cause of CNS infection in AIDS pts
T. gondii
Most common cause of intraocular inflammation & posterior uveitis in immunocompetent pts WW
T. gondii
Transmission of T. gondii
cat feces, undercooked pork
Primary Toxoplasmosis Sx
asymptomatic, cervical LAD or fever, fatigue, chills, HA, sore throat, mono-like Sx
Severe Primary Toxoplasmosis Sx
Mono-like Sx, lymphadenitis, retinochoroiditis, myocarditis, polymyositis, uveitis, hepatitis, or pneumonia
Primary Toxo, Acute Ocular Toxoplasmosis Sx
red eye, blurred or reduced vision, eye pain, photophobia, tearing, floaters; progression to Retinochoroiditis
incubate period of T. gondii
5-20d
Retinochoroiditis Sx
sudden or gradual impaired vision d/t yellowish-white cotton patch lesions on retina
Latent T. gondii infection
pseudocysts remain in tissues (lymph nodes, brain, eyes, lung, & muscle)
Congenital Toxoplasmosis Risk of fetal infection
female acquires primary infection DURING pregnancy, esp 2nd or 3rd trimester higher risk for infection
Congenital Toxoplasmosis Risk of fetal disease
female acquires primary infection DURING pregnancy, esp 1st or 2nd trimester higher risk of disease
Congenital Toxoplasmosis S/S
stillbirth, spontaneous abortion, hydrocephalus, encephalitis, retinochoroiditis, HSM, lymphadenitis, fever, atypical pneumonia, rash, diarrhea, jaundice, splenomegaly
Gold Standard Diagnostic test for Toxoplasmosis
Sabin-Feldman IgG Dye test
Other Diagnostic tests for Toxoplasmosis
IFA, TORCH, IgG/IgM Avidity test
Treatment for Toxoplasmosis, only targets actively dividing organisms
Pyrimethamine & Sulfonamides
Tx for 1st trimester pregnant female w/ Toxoplasmosis or Congenital
Spiramycin
Schistosoma mansoni
WW, feces shedding
Schistosoma japonicum
Orient, feces shedding
Schistosoma haematobium:
Africa, Asia, Portugal, Urine shedding
Schistosoma characteristics
Blood flukes/helminths, diecious
Life Cycle of Schistosoma
Cercariae penetrate human hair follicles -> in humans, schistosomulae migrate through the lungs to the hepatoportal system -> mature, mate, produce ova in the mesenteric v.
Immune response to Schistosoma
Humoral (IgE), ADCC (eosinophils)
Schistoma evades immune reponse by
Acquisition of blood group & host antigens on surface, masking them from host immunity; Metabolic products from adult inhibit T cell proliferation
Vector of Schistoma
snail
Primary Schistoma Sx
Schistosomal dermatitis: itchy papular eruption
Lung Involvement Schistoma Sx
Eosinophilic infiltration; Peripheral eosinophila; Acute phase exposure Sx: fever, n/v, abdominal pain, diarrhea – a syndrome known as “Katayama fever”
“Katayama fever”
fever, n/v, abdominal pain, diarrhea d/t Schistoma larvae traveling through lungs
Chronic Stage of Schistoma
Toxic hepatitis, irregular fluctuating fever, urticaria; intestinal hemorrhage & pseudodysentery; Eosiniophilic granulomatous (Th2) response to ova in liver and local tissue -> HSM, pulmonary schistomiasis, ascites
Schistosome Dermatitis aka “Swimmer’s Itch”
Schistosoma species that have an animal other than humans as a definitive host (waterfowl), may enter humans -> larvae die -> severe allergic dermatitis at site of penetration
Tx for Swimmer’s Itch
antihistamines, corticosteroids
Diagnosis for Schistoma
Presence of ova in GI/liver biopsy or fecal sample
Labs for Schistoma
high IgE & eosinophilia
Treatment for Schistoma
Praziquantel
Major Agents of Osteomyelitis
S. aureus & CoNS; GNRs, GAS, GBS, Anaerobes
Osteomyelitis + Sickle Cell
Salmonella
Osteomyelitis + Children
S. aureus, GAS, H. influenza, Kingella kingae
Osteomyelitis + Unregulated Diabetic
Mucomycoses
Osteomyelitis + Chronic, persistent, recurrent d/t SCV
S. aureus, P. aeruginosa, E. coli
Osteomyelitis + Immunocompromised
Aspergillus, MAC, Candida
Osteomyelitis + puncture wound
P. aeruginosa
Osteomyelitis causes
Trauma or surgery to bone or surrounding ST; Foreign body (artificial joint, pins, plates) for biofilm formation; Bacteremia or ST infection (cellulitis); IVDU or Nosocomial infections
Osteomyelitis caused by trauma/surgery Sx
Fever, chills, malaise, bone pain, swelling/pain of ST overlying affected bone
Osteomyelitis d/t Diabetic Foot most often affects which bones
Metatarsal head, Tarsal bone, Phalange involvement
Osteomyelitis d/t bacteremia
Fever, chills, malaise, bone pain, localized pain & swelling of ST
Children’s Osteomyelitis d/t bacteremia most often infects
metaphyseal areas of long bones – tibia, femur (Brodie Abscess – tibia osteomyelitis)
Adult’s Osteomyelitis d/t bacteremia most often infects
infects vertebrate (fever + back pain)
Radiographs: (+) several weeks post initiation of infection
Focal loss of trabecular pattern, periosteal reaction & frank bone destruction
What imaging modalities identifies Osteomyelitis earlier
CT, MRI +/- contrast, Bone scan (inflammation)
Tx for Osteomyelitis
prolonged Tx w/ ABX
Agents of SA in Children < 4y/o
S. aureus, GBS, GAS, S. pneumo, GNRs
Agents of SA in Children > 4y/o
S. aureus, CoNS, GAS, Enterococci,
N. gonorrhoeae, GNRs
Agents of SA in Elderly
GBS, GAS, S. pneumo, Peptostreptococcus, anaerobic & facultative anaerobic GNRs (Bacteroides), Candida
Agents of SA in Subacute or Chronic SA
MTB, Coccidioides immitis, Bastomyces dermatitis, Borrelia burgdorferi, T. pallidum
Agents of SA in Immunodeficient pts (hypogammaglobulinemia) esp during bacteremia
Mycoplasma & Ureaplasma
Viral Agents of SA
Hep B, Rubella, HPV-B19. Mumps
Viral Agents of SA act via
direct or cause a Type III HSN
> 24mo post-surgery - hematogenous dissemination acquired from sepsis, skin infection, or urosepsis; agent causing SA
S. aureus
Pathogenesis of SA
PMNs respond to joint infection -> release degradative & lysosomal enzymes; Bacteria also release exotoxins & degradative enzymes
Damage to the articular cartilage occurs -> effusion
Prosthetic joints pathogenesis of SA
-> biofilm S. aureus
Acute SA Sx
fever + joint pain, limited movement, tenderness, swelling of joint
Disseminated Gonococcal Infection -> SA Sx
occurs in untreated gonorrhea, several days after onset of genital infection
Fever, joint Sx, rash
Granulomatous Arthritis
insidious onset, slow progression w/ granuloma formation
Diagnosis of SA - Arthrocentesis
o (+) Culture o WBCs elevated (25,000-100,000) • PMNs if extracellular bacteria • Monocytic if viral, MTB, mycoses o RBCs may be present o Reduced glucose o Elevated protein & lactate
Diagnosis of SA - X-ray
ST swelling, joint-space widening, displacement of tissue planes by distended capsule
Tx for SA
IV Tx for ~1wk, then oral Tx if compliance is guaranteed
Agents causing RA
- RT infection: Chlamydia & Mycoplasma
- GU infection: Chlamydia & N. gonorrhoeae
- GI infection: Campylobacter, Yersinia, Salmonella, Shigella
Incubation of RA
S/S occur 7-14d post-infection
Risk Factors for RA
Male, HLA-B27
RA Sx
Arthralgias: painful, asymmetric, involving < 3-4 joints, but only 1 at a time, typically involving LE joints
Acute conjunctivitis, sterile urethritis, afebrile (unless mucosal infection causes fever)
Diagnosis of RA - Arthrocentesis
o (-) Culture o WBCs elevated (2,000-50,000) • PMNs o RBCs may be present o Elevated Abs, complement, protein o Normal glucose level
Diagnosis of SA - X-ray
ST swelling, joint-space widening, displacement of tissue planes by distended capsule
HIV-M Clade C
accounts for 50% of infections WW
HIV-M Clade B
predominates in US
HIV characteristics
ssRNA (+) sense
HIV 3 genes
gag, pol, env
GP120 – Surface Glycoprotein function
envelope protein that mediates attachment w/ the host cell’s CD4
GP41 – Transmembrane Glycoprotein function
envelope protein that mediates fusion of the viral envelope w/ the cytoplasmic membrane
Gag
encodes for matrix, capsid, nucleocapsid
Pol
encodes RT, protease, integrase
Env
encodes envelope glycoproteins GP120 & GP41 for attachment & fusion w/ host cells
Co-receptors for CD4/GP120
CCR5 or CXR4
GP120 binds CD4 on
T-helper cells, monocytes, macrophages, & dendritic cells
M-Tropic HIV (R5 strain):
cause the Primary Infection by binding to CCR5 co-receptor found on CD4 T cells, macrophages, monocytes, dendritic cells; Do not form syncytia – non-syncytia producing (non-SI)
T-Tropic HIV (X4 strain):
conversion as the infection proceeds by binding to CXCR4 co-receptor found on naïve CD4 Th cells; Form syncytia – (SI)
DC-SIGN
dendritic cell ICAM that typically binds CD40 during Tcell activation, is bound by GP120 -> increased half-life & increases the affinity of HIV-1 glycoproteins for CD4 (it presents HIV to the T cell in lymph nodes
Viremia peaks in blood 4-6 weeks after infection
coincides w/ CD4+ T cell reduction
Seroconversion takes place ~4-6wks
Abs cause plateau of viremia -> rebound in CD4+ T cell count, but not back to normal
Stage 1: HIV
(+), CD4+ T cell count > 500, CD4+ T cell % >29
Stage 2: HIV
HIV (+), CD4+ T cell count 200-499, CD4+ T cell % 14-28
Stage 3: AIDS
HIV (+), CD4+ T cell count <14
Immune response to HIV
Neutralizing Antibodies + Cytotoxic T Lymphocytes (CTL)
Sx of Primary HIV infection
10-20% w/ Sx: Fever, fatigue, rash, LAD, pharyngitis, arthralgia, n/v, diarrhea, night sweats, HA, etc; Sx resolve in ~2weeks
Latent HIV Sx
No S/S, reduced CD4+ T cell count (500-1000)
Opportunistic Infections in AIDS pts
o Toxoplasma gondii o Cryptosporidium parvum o Pneumocystic jiroveci o Candida o Cryptococcus neoformans o Histoplasma capsulatum o MTB o MAC o Salmonella o Bartonella o CMV, HSV, EBV, HHV-8, HPV, Poxvirus, JC virus
Diagnosis of HIV
P24 antigen: present 2-3 weeks after infection
HIV Abs: 4-6wks
Window Period of HIV:
period before Ab production where viremia is present, only marker is p24
Confirmatory test for HIV
ELISA to detect Ab against HIV
Monitor HIV Tx w/
CD4+ T cell levels: Flow Cytometry
Viremia: rtPCR to quantify viral RNA presence in blood
Genotypic and Phentypic tests can determien
if there was a recent mutation in the HIV
ART drugs
RT Inhibitors (NRTI, NNRTI), Protease inhibitor, Fusion inhibitor, Integrase strand transfer inhibitors
RT Inhibitors NRTI
Nucleoside analogue RT inhibitor (NRTI): gets incorporated into the growing DNA chain & causes termination
RT Inhibitors NNRTI
Non-Nucleoside analogue RT inhibitor (NNRTI): cause chain termination w/o getting incorporated into DNA
Protease inhibitor
Prevent protease from cleaving viral proteins; Irreversible
Fusion inhibitor
Inhibit p41 to block fusion of virus and host cell
Integrase strand transfer inhibitors
Effective when used in combination w/ other ARTs
HAART recommendations
2 RTIs + a PI (old recommendation)
2 NRTIs + NNRTI/PI/INSTI
ART therapy for HIV
Asymptomatic Pts w/ CD4 < 500
All symptomatic Pts
