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Infectious Disease > Bacterial Infections 2 > Flashcards

Bacterial Infections 2 Flashcards

1
Q

bacterial infections

A

-rheumatic fever
-tetanus
-salmonellosis
-poststreptococcal glomerulonephritis
-botulism
-shigellosis
-sepsis
-camplobacter jejuni
-diphtheria

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2
Q

rheumatic fever

A

-rheumatic fever (acute rheumatic fever) can affect the heart, joints, brain, and skin
-can develop if strep throat and scarlet fever infections are not treated properly
-early dx and treatment with antibiotics are key to preventing
-A. Streptococcus or group A strep cause strep and scarlet fever
-usually takes about 1-5 weeks after strep or scarlet fever for it to develop
-thought to be caused by a response of the body’s defense response/immune system
-immune system responds -> generalized inflammatory response

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3
Q

signs and symptoms of rheumatic fever

A

-fever
-painful, tender joints (arthritis), most commonly in the knees, ankles, elbows, and wrists -> migratory polyarthritis
-symptoms of congestive heart failure, including chest pain, shortness of breath, fast heartbeat
-fatigue
-jerky, uncontrollable body movements (called chorea)
-painless lumps (nodules) under the skin near joints (rare symptom)
-raised rash that appears as pink rings with a clear center (rare symptom) -> erythema marginatum
-can also have: carditis
-new heart murmur
-enlarged heart
-fluid around the heart

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4
Q

rheumatic fever testing

A

-no single test to dx
-look for signs, hx, and use many tests like:
-throat swab to look for group A strep infection
-blood test to look for antibodies showing recent group A strep infection
-heart function -> electrocardiogram (ECG)
-heart muscle -> echocardiogram or echo

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5
Q

rheumatic fever treatment

A

-treat symptoms with medicines like aspirin to reduce fever, pain, and general inflammation
-antibiotics to treat group A strep infections
-rheumatic heart disease- if symptoms of heart failure -> treat this
-rheumatic heart disease weakens the valves between the chambers
-severe rheumatic heart disease can require heart surgery and result in death

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6
Q

rheumatic fever prevention

A

-treat group A strep infections with antibiotics
-prevent group A in the first place
-use preventive antibiotics for people who had rheumatic fever in the past -> prophylaxis or secondary prevention
-may need antibiotic prophylaxis over a period of many years (often until 21) -> can include daily antibiotics by mouth or shot into muscle every few weeks

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7
Q

shigella

A

-aka bacillary dysentery
-causative agent- four serogroups of shigella, broken down into group A: S. dysenteriae; Group B: S. flexneri; Group C: S. boydii; and group D: S. sonnei
-transmission is fecal-oral
-very small inoculum of bacteria required for transmission -> spreads easily -> food, water, closed spaces
-incubation- 1-7 days, average 3 days
-geographic regions affected- worldwide, more common in developing nations

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8
Q

shigella signs and symptoms

A

-acute bacterial hemorrhagic diarrheal illness
-caused by any one of 4 shigella serogroups
-diarrhea, fever, abdominal pain and cramps, tenesmus (feeling like you have to pee) , malaise nausea and vomiting
-diarrhea is initially watery and nonbloody then become mucoid and bloody as the infection transitions into the large bowel
-symptoms typically last 5-7 days without treatment
-complications can include hemolytic uremic syndrome (HUS), seizures in children, and reactive arthritis

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9
Q

shigella diagnosis and treatment

A

-should be suspected in pts presenting with bloody diarrhea, abdominal pain, fever, and small, frequent stool volumes
-stool can be cultured or tested using PCR
-antibiotics can reduce the duration of symptoms in infected pts
-bc antibiotics resistance to TMP/SMX and ampicillin is commonplace -> current recommendation call for either azithromycin or ciprofloxacin
-providers should be aware of emerging resistance to these antibiotics as well
-antispasmodics should be avoided

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10
Q

types of shigella and severity

A

-shigella is most infectious bacterial diarrheal disease, commonly passes via person to person transmission
-S. dysenteriae serotype 1 (formerly Shigella shigae) tends to be a more aggressive pathogen, whereas S. sonnei tends to cause milder disease
-S. sonnei is more common in developed nations, and S. flexneri is more common is less developed nations

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11
Q

shigella prevention

A

-carefully wash hands
-avoid swallowing water from ponds, lakes, or untreated swimming pools
-traveling -> follow safe food and water guidelines
-avoid sexual activity with those who recently (several weeks) recovered from shigellosis

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12
Q

salmonella

A

-caused by nontyphoidal Salmonella
-causative agents- Salmonella bongori, Salmonella enterica
-reservoir- poultry is most common, some reptiles
-typically foodborne via undercooked poultry, raw eggs, peanut butter, ice cream, reptiles
-incubation- 12-48 hrs
-geographic- worldwide

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13
Q

salmonella signs and symptoms

A

-acute, febrile, bacterial diarrheal illness
-transmitted by undercooked poultry (chicken/raw eggs) and characterized by watery and/or bloody diarrhea
-fever, malaise, nausea, vomiting, abdominal pain/cramps, tenesmus, and diarrhea
-bloody diarrhea can also occur -> more common in children
-often self limiting
-symptoms typically resolve within 3-7 days
-more severe infections are seen with larger bacterial inoculums, in young children and older adults and the immunocompromised
-may become invasive and can cause bacteremia, meningitis, septic arthritis, and osteomyelitis (sickle cell pts are at increased risk)
-postinfectious IBS and reactive arthritis may occur in some pts

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14
Q

salmonella diagnosis and treatment

A

-stool culture - gold standard
-supportive treatment and consists of fluids and a gentle diet
-antibiotics are indicated in cases of severe illness, persistent fever, hig hrisk pts (old age, weakened immune system), and those with invasive disease
-fluoroquinolones (ciprofloxacin or levofloxacin), macrolides (azithromycin), or cephalosporins (ceftriaxone or cefotazmine)
-resistance to TMP/SMX and other antibiotics is on the rise

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15
Q

diphtheria

A

-caused by Corynebacterium diphtheriae
-incubation- 2-5 days
-geographic regions- worldwide, rare in US bc vaccine
-bacterial infection of respiratory tract caused by C. diphtheriae
-a gram positive, pleomorphic, toxin producing bacteria
-can occur anywhere from nasopharynx to the tracheobronchial tree
-tonsils and oropharynx (tonsillopharyngeal) the most common sites of infection
-known for its characteristic gray pseudomembrane
-may be asymptomatic carriers after exposure

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16
Q

tonsillopharyngeal diphtheria signs and symptoms

A

-progressive symptoms
-begin as odynophagia, pharyngeal erythema, and sore throat
-low grade fever, chills, malaise, fatigue, worsening pain, and lymphadenopathy follow
-characteristic gray pseudomembrane comprised of WBCs, fibrin, dead tissue often forms
-membrane can spread through the respiratory tract, causing more significant symptoms

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17
Q

nasal diphtheria signs and symptoms

A

-involvement of the nasopharynx is characterized by nasal congestion and mucopurulent, bloody nasal discharge

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18
Q

laryngeal diphtheria signs and symptoms

A

-if the pseudomembrane extends down into the larynx, “diphtheritic croup” can occur, potentially causing respiratory compromise
-barking cough, stridor, hoarseness, significant neck swelling (bull neck), and may become hypoxic and cyanotic
-may spread hematogenoulsy and cause damage to the cardiac, renal, and/or nervous system

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19
Q

diphtheria diagnosis and treatment

A

-nasopharyngeal and oropharyngeal cultures should be obtained and plated on Loffler or Tindale media
-gram stain may reveal gram positive rods in chinese character distribution
-polymerase chain reaction (PCR) and enzyme linked immunosorbent assay (ELISA) antigen tests can be used to detect diphtheria toxin
-pts should be put in isolation
-antibiotics and horse serum based antitoxin are the mainstay of treatment
-antibiotic choices include eryhtromycin or penicillin for 14 days
-pts are not infectious after 48 hours of antibiotic therapy
-antitoxin can be obtained from CDC and dosing is based on stage and severity

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20
Q

tetanus

A

-aka lockjaw
-causative agent- clostridium tetani
-incubation- 3-21 days, average 10 days
-geographic regions- worldwide, more common in developing nations where less vaccination is available
-muscle spasms
-caused by gram positive, anaerobic bacteria C. tetani
-bacteria commonly found in soil and manure
-4 forms:
-generalized
-localized/wound tetanus
-neonatal tetanus
-cephalic tetanus

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21
Q

tetanus signs and symptoms: generalized

A

-most common (80%)
-often presents as trismus (lock jaw) or risus sardonicus
-muscle spasms that develop in descending pattern
-pts may develop sympathetic hyperactivity, laryngospasm, and opisthotonus (clenched fists, flexed arms, arched back, and extended legs)
-mortality- 10-20%

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22
Q

localized tetanus: signs and symptoms

A

-mild form
-localized muscle spasm in close proximity to wound
-more common in partially immunized pts
-low mortality

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23
Q

neonatal tetanus: signs and symptoms

A

-highest mortality rate
-results from contamination of infants umbilical stump with dirt or bacteria laden matter
-first exhibit poor feeding and later progress to full blown tetanus

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24
Q

cephalic tetanus: signs and symptoms

A

-rarest form
-short 1-2 day incubation
-results from head or neck wound
-unlike the other forms -> does not cause muscle spasm/tetany -> presents as unilateral facial nerve palsy

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25
Q

tetanus testing and treatment

A

-based on clinical findings and hx of wound infection in an unvaccinated or undervaccinated pt
-tetanus immune globulin should be given to sequester unbound toxin and vaccination with tetanus toxoid should be initiated
-wound debridement, wound care, and antibiotic administration
-may require intubation to secure the airway and provide ventilation
-benzodiazepines and/or neuromuscular blocking agents for muscles spasm

26
Q

botulism

A

-causative agent- clostridium botulinum- botulism toxin
-incubation- food borne: 6hrs-10days (average 12-36 hrs); wound: 4-14days
-geographic regions- worldwide
-rare paralytic illness
-toxin produced by gram positive spore forming, bacillus shaped, obligate anaerobic bacteria C. botulinum
-commonly as a result of ingestion of toxin (Food) or spores (infant)
-infant- spores colonize GI tract and produce toxin
-less common- wound infection (usually IM or IV drug use), spore inhalation, iatrogenically (botox)

27
Q

signs and symptoms: food borne botulism

A

-food borne- acute onset bilateral facial palsy and descending weakness in absence of fever
-mental status intact
-blurry vision, bradycardia, GI symptoms such as nausea, vomiting, diarrhea, and abdominal pain may be present

28
Q

infant botulism signs and symptoms

A

-floppy baby syndrome
-may have weak cry, poor feeding, drooling, weakness, and constipation
-absence of fever

29
Q

wound botulism signs and symptoms

A

-similar presentation to food borne botulism
-NO GI symptoms
-pt still exposed to circulation toxin from the wound, but their GI tract is spared exposure
-fever may be present secondary to wound infection

30
Q

botulism diagnostic testing

A

-hx, clinical presentation, electromyogram (EMG) testing suggest the dx
-infant botulism confirmed via isolation of infectious spores and botulin toxin in stool samples
-food borne botulism in adults confirmed via detection of botulin toxin in serum, stool, vomitus, or suspect food specimens
-pts with wound botulism -> detectable toxin in their serum but not stool (no GI tract involvement)

31
Q

botulism treatment

A

-supportive
-intubation and mechanical ventilation as indicated
-horse serum based antitoxin available for adults and children 12 mo or older
-human derived botulism immune globulin available for infants < 12 mo
-antibiotics for wound botulism -> no effect of food borne of infant
-use caution with home canning
-discard dented or bulging cans
-do not feed children less than 1 honey-> may contain botulism spores

32
Q

campylobacter jejuni

A

-causative agent- campylobacter jejuni, campylobacter coli
-reservoir- GI of animals, poultry most common
-transmission- foodborne via consumption of undercooked poultry, raw, fecal oral of symptomatic people
-incubation- 1-7 days, average 3 days
-geographic regions- worldwide
-acute, febrile, bacterial diarrhea illness
-characterized by watery diarrhea that frequently becomes bloody after a few days

33
Q

campylobacter jejuni presentation

A

-may have febrile prodrome before diarrhea occurs
-fever, malaise, abdominal pain/cramps, tenesmus, watery diarrhea that often becomes bloody
-nausea and vomiting may occur in some pts
-illness is often self limiting and symptoms typically resolve within 7 days
-acute setting-> pts may develop right lower quad abdominal pain prior to onset of diarrhea (pseudoappendicitis)
-postinfectious complications can be Guillain-Barre syndrome and reactive arthritis

34
Q

campylobacter jejuni dx and treatment

A

-Stool culture - gold standard
-Darkfield or phase-contrast microscopy may reveal motile, gram-negative, curved/helical-shaped rods
-stool antigen and PCR tests available
-mainstay of treatment is supportive and consists of fluids and a gentle diet
-antibiotics decrease duration of illness -> azithromycin 500 mg daily × 3 days or erythromycin 500 mg four times daily × 5 days
-worldwideresistance to fluoroquinolones, specifically in Southeast Asia

35
Q

Group A streptococcus

A

-aka strep throat
-causative agent- group A streptococcus (GAS)
-incubation- approx 2-5 days
-geographic regions- worldwide
-strep throat most common form of bacterial pharyngitis and peaks late winter and early spring
-complication of strep throat- rheumatic fever, poststreptococcal glomerulonephritis, and peritonsillar abscess

36
Q

group A streptococcus dx and signs

A

-rapid strep test (RADT- rapid antigen detection test) and throat culture
-symptom onset is acute -> fever, anorexia, malaise, sore throat, headache, abdominal pain, nausea, and vomiting
-on exam- enlarged tonsils with or without exudate, pharyngeal erythema, oral petechiae, and enlarged tender cervical lymphadenopathy
-some may develop scarlatiniform rash
-cough notably absent

37
Q

group A streptococcus treatment

A

-lessen disease severity, transmission, and decrease likelihood of complications like rheumatic fever
-penicillins, amoxicillin, and cephalosporins are effective treatments
-erythromycin, clindamycin, or macrolides can be used in pts with penicillin allergy

38
Q

modified centor criteria

A

-applied to estimate the likelihood of strep pharyngitis
-points are added or subtracted based on risk factors to create a total scare
-ranges from -1 to 5
-higher the score the more likely pt has strep pharyngitis

39
Q

infective endocarditis

A

-causative agents- staphylococci and streptococci -> staphylococcus aureus, streptococcus viridans
-also HACEK- Haemophilus, Aggregatibacter, Cardiobacterium, Eikenell a, and Kingella-> small, fastidious, gram negative rods
-infectious process of inner lining of heart (mostly valves) typically caused by bacteria (bacterial endocarditis)
-short incubation period and present acutely
-may have more insidious and indolent course of progression and develop over several weeks
-risk factors- IV drug abuse, poor dentition, valvular heart disease, congenital heart disease, prosthetic heart valves, indwelling lines, pacemakers, past hx of infective endocarditis, and chronic hemodialysis

40
Q

infective endocarditis presentation

A

-fever most common presenting symptom associated with chills, fatigue, and malaise
-heart murmur is present in up to 85%
-may also myalgia, arthralgia, splinter hemorrhages, septic emboli, petechiae, splenomegaly, cough, weight loss, and/or glomuleronephritis
-Janeway lesions, Osler nodes, and Roth spots -> highly suggestive of bacterial endocarditis
-Janeway lesions are nontender erythematous macules on the palms and soles
-osler nodes are painful, purplish-red lesions found on the pads of the fingers
-roth spots are retinal hemorrhages with pale centers

41
Q

infective endocarditis diagnosis

A

-should be considered when pt with any of the listed risk factors present with fever, heart murmur, and clinical signs and/or symptoms supporting the dx
-blood cultures should be obtained from at least 3 different sites and an echocardiogram, preferably transesophageal, should be performed looking for valvular vegetations
-labs may show elevated C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and rheumatoid factor

42
Q

infective endocarditis treatment

A

-empiric treatment should be initiated in acutely ill pts once blood cultured have been obtained
-vancomycin and ceftriaxone or gentamycin -> first line agents until a more tailored regimen can be provided based on blood culture results
-if pts are not acutely ill or in heart failure -> treatment can be withheld until blood cultures are resulted
-if initial round of blood cultures is negative -> 2-3 more sets should be drawn prior to initiation of empiric treatment

43
Q

sepsis

A

-defined as systemic inflammatory response in association with a confirmed or strongly suspected infection
-inflammation response is commonly referred as systemic inflammatory response syndrome (SIRS)
-defined clinically by more than one of the following:
-core body temp > 38 or <36
-heart rate above 90bpm or greater than 2 standard deviation from age appropriate normal
-respiratory rate greater than 20 breaths per minute or hyperventilation
-measured peripheral WBC of greater than 12,000 or less than 4000

44
Q

severe sepsis

A

-sepsis but also includes:
-organ dysfunction- renal failure, respiratory failure, delirium
-hypoperfusion- lactic acidosis
-hypotension- absolute systolic blood pressure below 90 or greater than 40 below the pt baseline systolic

45
Q

septic shock

A

-severe sepsis but also persistent hypotension
-despite aggressive fluid resuscitation that requires cardiovascular support measures (vasopressors, steroids)

46
Q

risk factors: gram positive bacteria

A

-normal or immunosuppressed host
-asplenia susceptible to encapsulated gram positive bacteria like Streptococcus pneumonia

47
Q

risk factors gram negative bacteria and fungi

A

-immunosuppression (chronic corticosteroid use, chemotherapy, solid organ, or stem cell transplantation, neutropenia)
-chronic medical conditions (hemodialysis, diabetes, cirrhosis)
-indwelling catheters

48
Q

risk factors for anaerobic bacteria

A

-uncommon
-traumatic injuries
-invasive disease to cause necrotizing skin and soft tissue infections
-costridium

49
Q

cause of sepsis

A

-infectious causes of SIRS:
-bacteremia- IV devices, pulmonary infections, intra-abdominal infections, endovascular infections, or UTI
-vascular access, or intravascular device associated infection
-lower respiratory tract infection- pneumonia or empyema
-intra-abdominal infection- peritonitis, cholecystitis, diverticulitis/abscess, pancreatic abscess, septic abortion, or Clostridium difficile colitis
-UTI- cystitis, pyelonephritis, renal abscess, or foley catheter related infection
-endovascular infections- endocarditis or vascular graft infections
-skin and soft tissue infection- necrotizing fasciitis, soft tissue abscess or surgical site infection

50
Q

sepsis signs and symptoms

A

-fevers, chills, and/or rigors
-irritability, confusion, or lethargy
-tachypnea, hypoxia, acute respiratory distress, or respiratory failure
-hepatic and/o renal failure

51
Q

sepsis testing

A

-lab- no diagnostic gold standard
-1. CBC with diff cell count- leukocytosis may suggest infection, but elevated neutrophil count (left shift) lacks sufficient sensitivity to differentiate infectious from noninfectious for sepsis
-thrombocytosis may be associated with infection due to yeast or mold
-2. basic metabolic panel- nonspecific, routinely ordered, results of serum creatinine level may affect antimicrobial dosing
-3. liver enzymes and coagulation test (PT/PTT/INR)- biliary tract infections may be associated with elevated alkaline phosphatase and total bilirubin levels. Coagulation studies can be abnormal with sepsis but nonspecific with elevated values suggesting disseminated intravascular coagulation (especially with decreased fibrinogen)
-4. serum lactate- levels > 4 may suggest tissue hypoperfusion and need for fluid resuscitation, but sepsis is associated with increased glycolysis and increased serum lactate production
-5. urine microscopy and urine culture- fever and/or UTI in association with hematuria and pyuria (at least 10 WBCs/cmm) and bacteriuria may suggest cystitis, pyelonephritis, or renal abscess
-6. blood culture- 2 sets of blood cultures prior to initiation of antimicrobial therapy. 1 set percutaneous site and 1 set through vascular access site that has been in place for > 48 hrs
-7. sputum gram stain and culture- routine culture with sepsis pt and purulent respiratory sections
-8. wound or abscess cultures- superficial swab NOT recommended -> needle aspirated contents from intact bulla or vesicles and deep cultures from abscesses, surgical wounds, or pressure ulcers
-9. stool studies- eval for CLostridium difficile colitis
-10. ESR, C-reactive protein (CRP) and procalcitonin (PCT)- nonspecific test that is elevated with infection/inflammation. Systemic PCT production has been shown to be relatively specific to bacterial infections and sepsis
-PCT between .5-2.0 make sepsis possible at these levels but are also associated with noninfectious conditions
-PCT 2-10 are suggestive of sepsis
-PCT < 0.5 pts without sepsis

52
Q

radiological studies for sepsis

A

-plain film abdominal and chest imaging- rarely yield dx; chest image may be helpful to identify pneumonia and abdomen may indicate free air (bowel perforation with peritonitis) or presence of gas within an abscess cavity
-CT scan- chest and abdomen are more sensitive for CT and evaluation pneumonia and intra-abdominal abscess (2 most common causes)
-echocardiography- transthoracic (TTE) or transesophageal (TEET) review of dule criteria and evaluate endocarditis
-ultrasonography- noninvasive evaluation of biliary tract or pelvic etiologies

53
Q

sepsis treatment

A

-early goal directed therapy and initials resuscitation -> initial fluid resuscitation
-maintain a central venous pressure (CVP) of 8-12 mmHg
-maintain a mean arterial pressure (MAP) of > 65 mmHg
-maintain central venous oxygenation > 70%
-vasopressor and inotropic support for cardiovascular status and perfusion -> norephinephrine and dopamine
-corticosteroid therapy- persistent hypotension despite initial fluid resuscitation and vasopressor and inotropic support may benefit for functional adrenal insufficiency
-blood product administration- transfuse packed RBCs if Hmg is < 7.0. Platelets should be transfused for any significant amount of bleeding or if count is < 5,000
-glucose control- insulin therapy should be initiated for glucose > 150 (improves neutrophil function)

54
Q

sepsis antibiotic treatment

A

-prompt initiation of broad spectrum antimicrobial therapy
-combination regimen that covers gram positive and negative within first hour of sepsis -> increase survival
-no standard regimen exists, its suggested:
-1. ceftazidime 2g IV q8 hours or cefepime 2g IV q8 hours or doripenem 500mg IV q8
-2. daptomycin 6 mg/kg IV q 24 hours or linezolid 600 mg IV q 12 hours or vancomycin 15 mg/kg IV q 12-24 hrs
-3. guidelines suggest a duration of antimicrobial therapy for sepsis to be 7-10 days -> BUT monitor daily and adjust for renal function and comorbid conditions, drug intolerance, susceptibility pattern of isolated pathogen, underlying infectious disease process

55
Q

sepsis prevention

A

-source identification and control
-within first 6 hours -> Source should be identified to identify pts that may benefit from timely and effective intervention
-conditions that benefits from early intervention:
-prompt removal of an infected vascular access device -> central venous catheter, urinary foley catheter
-percutaneous or surgical drainage of deep space infection- intra-abdominal, intrathoracic, or intracranial abscess, joint space infection, or necrotizing skin and soft tissue infection

56
Q

methicillin-resistant staphylococcus aureus (MRSA)

A

-impact pts who have no been recently (<1yr) hospitalized or had medical procedure (dialysis, surgery, catheters)
-causes mild to moderate SSTIs (abscesses, furuncles, and carbuncles)
-severe or invasive CA-MRSA disease is less frequent but can include:
-osteomyelitis
-sepsis
-septic thrombophlebitis
-necrotizing fasciitis
-necrotizing pneumonia with abscesses
-HA-MRSA can still cause SSTIs in community but LESS frequent
-affects skin and soft tissue

57
Q

MRSA risk factors

A

-50% no risk factors
-other risk factors include:
-antibiotic use in past month, particularly cephalosporin and fluoroquinolone
-abscess
-reported spider bite
-intravenous (IV) drug use
-HIV infection
-hemodialysis catheter
-hx of MRSA infection
-close contract with similar infection
-children
-resident in long term care facility

58
Q

MRSA treatment

A

-wound culture- definitive diagnosis
-wound culture of purulent lesion with systemic signs of illness or if the pt is immunocompromised
-ultrasound may help identify abscess
-consider surgical drainage, wound culture, narrow spectrum antimicrobial for purulent infections
-antibiotics active against MRSA for pts with carbuncles or abscesses
-if pts do not respond to initial antibiotic -> have markedly impaired host defenses
-modify therapy based on culture and susceptibility
-treat underlying condition (tinea pedis)
-restrict contact (sports competition) if wound cannot be covered
-elevated affected area

59
Q

descending vs ascending pain

A

-starts at center and radiates towards limbs -> descending
-ascending starts at limbs and radiates inwards

60
Q

macules

A

-flat

Infectious Disease (10 decks)

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