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Clinical Medicine 1 > Lecture 4 (ID)-Exam 2 > Flashcards

Lecture 4 (ID)-Exam 2 Flashcards

1
Q
  • A lot of times fever goes along with with what?
  • What prompts diagnosis & institution of life-saving therapy or critical infection-control interventions?
A
  • Acutely ill patient with fever & rash diagnostic challenge
  • Distinctive appearance of an eruption with clinical syndrome facilitates prompt diagnosis & institution of life-saving therapy or critical infection-control interventions.
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2
Q

What are certain things you need to ask or obtain from the patient (11)?

A
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3
Q

What are the different distribition/characterisitic of rash? (9)
* which rash is the most common?

A
  • Centrally distributed maculopapular-> MC
  • Peripheral
  • Confluent desquamative erythematous
  • Vesiculobullous
  • Urticarial
  • Nodular
  • Purpuric
  • Ulcerated
  • Eschars
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4
Q

What is the most common type of eruption?
* describe the rash?

A

Centrally Distributed Maculopapular Eruptions
* Most common type of eruption
* Centrally distributed rashes, in which lesions primarily truncal

trunk, not face and limbs

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5
Q

What rash is this?

A

Centrally Distributed Maculopapular Eruptions

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6
Q

What are the reasons for centrally distibuted maculopaular eruptions?

A
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7
Q

What are infectious exanthem?

A

Pink macules & papules becoming confluent in some areas

rash of the outer side (skin)

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8
Q

What rash is this?

A

Infectious Exanthem

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9
Q

What are peripheral eruptions?

A

These rashes are alike in that they are most prominent peripherally or beginning peripheral (acral) areas before spreading centripetally (unlike Centrally Distributed Maculopapular Eruptions)

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10
Q

What are examples of peripheral eruptions (6)

A
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11
Q

What are confluent desquamative erythemas?

A

These eruptions consist of diffuse erythema frequently followed by desquamation

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12
Q
  • What are some causes of confluent desquamative erythemas? (4)
  • What do you need to treat this as?
A
  • Scarlett Fever postScarlett
  • Streptococcal/Staphylococcal Toxic Shock Syndrome
  • Kawasaki Disease
  • SJS/TEN
  • Need to treat it like a burn with fluids and antibioics
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13
Q

What rash is this?

A

Confluent Desquamative Erythemas

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14
Q

What are vesiculobullous Eruptions? What are the causes? (2)

A

These eruptions consist of numerous lesions in multiple stages of evolution
* Varicella
* Echthyma gangrenosum

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15
Q

What rash is this?

A

Vesiculobullous Eruptions

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16
Q

What is urticarial eruption? What is it related to?

A
  • Showing characteristic discrete & confluent, edematous, erythematous papules (bump) & plaques (large patch)
  • Most likely are related to an I allergic or hypersensitivity type reactions

Allergy to nickle=belt pattern

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17
Q

What rash is this?

A

Urticarial Eruption

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18
Q
  • How does Purpuric Eruptions present?
  • Does it blanch or not?
A
  • Classically presents as petechial eruption, but initial lesions may appear as blanchable macules or urticaria.
  • Purpura does NOT blanch
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19
Q

What are the causes of purpuric eruptions? (4)

A
  • Acute Meningococcemia
  • Gonococcemia
  • Echovirus 9 infection
  • ITP/TTP
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20
Q

What are the typical pathogens (bacterial infections)?

A
  • S. aureus (C+)
  • S. epidermidis or S. saprophyticus (C-)
  • Strep. pyogenes
  • Group A beta-hemolytic strep
  • Group B & C and G strep
  • S. pneumoniae
  • H. influenza
  • Yersinia enterocolitica
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21
Q

What three organisms are the most common for URI and otitis?

A

Staph, strep and H.influ

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22
Q

What test is used for the difference between s.aureus and other staphylococcus species?

A
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23
Q

Skin and Soft Tissue Staph Infections:
* ~25% of people are asymptomatic carriers of what?
* How is it spread?
* Distinguish factors btw staph and strep?
* What are the types
* Rarely a cuase of what?
* What is the diagnosis?
* What is the txt?

A
  • ~25% of people are asymptomatic nasal carriers of S aureus
  • Spread by direct contact
  • Distinguishing factor between Staph and Strep – abscess formation common and typically more purulent
  • Folliculitis, Furuncles
  • Rarely a cause of necrotizing fasciitis
  • Diagnosis – culture wound
  • Treatment – I & D when appropriate, Oral or IV ABX
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24
Q

Methicillin-resistant Staphylococcus aureus (MRSA):
* What is the pathophysiology?
* The pathogenesis of MRSA in not completely understood – traditionally occurs where more?
* What has staph developed?

A
  • Pathophysiology – S. Aureus is able to thrive in biofilms on prosthetic devices, in epithelium, has a high enzyme production allowing it to invade and destroy host tissues and metastasize.
  • The pathogenesis of MRSA in not completely understood – traditionally occurs in hospital setting more often than in community.
  • Developed antibiotic resistance with few weapons in arsenal effective in fighting it
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25
Q

MRSA
* Outbreaks occurs in where?
* Occurs how?
* What is prevention?
* What is the diagnosis?
* What is the treatment?

A
  • Outbreaks occur in crowded places – locker rooms, etc.
  • Occurs in waves
  • Prevention – thorough cleansing of public areas, locker rooms, hand-washing
  • Diagnosis – culture
  • Treatment – Use antibiogram (local/regional etc.) to decide on sensitivity
    * Clindamycin, Trimethoprim-sulfamethoxazole (Bactrim), doxycycline
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26
Q

What is used for MRSA treatment (PO)

A

Clindamycin, Trimethoprim-sulfamethoxazole (Bactrim), doxycycline

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27
Q

What is cellulitis? What is it distinguished from?

A
  • Acute inflammatory condition of skin caused either by endogenous flora colonizing skin or by a wide variety of exogenous bacteria
  • Distinguish from folliculitis, furuncle and carbuncle
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28
Q

What are the ports of entry for cellulitis?

A
  • Organisms inoculated through small breaks in skin (S. pyogenes) or via bites (Bartonella - cats, Pastuerella - dogs, Eikenella - humans, anaerobes)
  • Originate in wounds, ulcers or abscesses (S. aureus)
  • Be associated with sinusitis( H. flu)
  • Gain entry during immersion in water (Aeromonas, Vibrio vulnificus)
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29
Q

What are the cellulitis clincial presentation/PE finding?

A
  • Shaking chills often occur but bacteremia infrequently documented
  • Regional LN enlargement & tenderness common
  • Linear streaks of erythema & tenderness indicate lymphatic spread
  • Characterized by localized pain, erythema, swelling & heat
  • Lymphangitis vs erysipelas
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30
Q

What is this? What is the cause?

A

Right: Strep
Left: Staph

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31
Q

Cat Scratch Disease/Fever
* What are the s/s?
* What population?
* What are teh more severe manifestations?

A
  • Painful regional lymphadenopathy that persists for several weeks or months after a cat scratch.
  • Since scratches most often occur on the hand or face in children, youngsters account for 60% of cases, so expect LAD in the same regions.
  • Systemic symptoms and even severe manifestations such as encephalitis, seizures, & coma may occur.
    * Trench fever (B. quintana) – fever, headaches, aseptic meningitis in a homeless person or soldier
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32
Q

What is Trench fever (B. quintana) ?

A

fever, headaches, aseptic meningitis in a homeless person or soldier
* Altered mental status with negative spinal tap

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33
Q

What is the DX and TX of cat scratch disease/fever?

A

Dx: LN biopsy or PCR serology tests for B. henselae
* Warthin-Starry silver stain

Tx: Azithromycin + doxycycline
* Azithromycin has been noted to be successful to reduce Lymph node size
* Ciprofloxacin in AIDS patients with bacteremia
* Alternatives: Sulfamethoxazole/trimethoprim, rifampin or clarithromycin

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34
Q

Vibrio Cellulitis (Non-cholera vibrio species)
* What are the different strains?
* What is it the cousin of?
* Where does it inhabit?
* What strain is most likely to cause skin infection and progress to necrotizing fasciitis and DIC?

A
  • Vibrio parahaemolyticus,V. mimicus,V. alginolyticus,V. hollisae, andV. vulnificus
  • Cousins of organism causing cholera (Vibrio cholerae)
  • Typically inhabit warm salt water or mixed salt and fresh water
  • V. vulnificus
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35
Q

What is the DX and TX of vibrio cellulitis?

A
  • Dx: noncholera Vibrio grow in cultures
  • Tx: Doxycycline + Cephalosporin (1st Gen)
    * Prophylax all high risk wounds
    * Think CD vid(brio)

Some sources say Ciprofloxacin + Cephalosporin

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36
Q

What bacteria does this show?

A

Vibrio Cellulitis (Non-cholera vibrio species)
* Vibrio parahaemolyticus, V. mimicus, V. alginolyticus, V. hollisae, and V. vulnificus

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37
Q

Cellulitis-Etiology

Lower extremity:
* What are the most common organisms (2)?

A
  • Group A B-hemolytic streptococci
  • S.aureus
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38
Q

Cellulitis-Etiology

What are the MC organisms for Neutropenic /immunosuppresed patients (2)?

A
  • Gram – bacilli
  • Always think Pseudomonas in DM (Also mc with pneumonia in CF pts)
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39
Q

Cellulitis-Etiology

What are the most common organisms for infected ulceration of skin (2)?

A
  • Anaerobic bacteria
  • Gram-
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40
Q

n children cellulitis of face or upper extremities often due to what organism?

A

H. flu

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41
Q

When should radiologic studies should be done with cellulitis?

A

Radiologic studies should be performed on patients with ulcers to R/O osteomyelitis
* Use MRI or Nuclear Med scan to see cellulitis or OM

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42
Q

What is the treatment of folliculitis? (mild and severe)

A
  • Moist heat
  • Avoidance of irritating factors
  • Antibacterial soaps
  • Topical antibiotics
  • Systemic antibiotics, if more extensive
    * Dicloxacillin
    * Cephalexin
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43
Q

What is furuncle? What is the most common organism?

A

Localized pyogenic infection, most frequently by Staphylococcus aureus, originating deep in a hair follicle. AKA furunculus, boil.
* involves sweat gland or hair follicle
* Larger than follicultitis

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44
Q

What is this? What is it caused by?

A

Furuncle-S.aureus

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45
Q

What is a carbuncle? When is a culture appropriate?

A
  • Deep-seated pyogenic infection of skin & subcutaneous tissues, usually arising in several contiguous hair follicles, with formation of connecting sinuses
  • Culture is usually not necessary unless patient has predisposing factors such as diabetes, IV drug use or HIV, or if there are systemic symptoms
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46
Q

What is this?

A

Carbuncle
* Deep-seated pyogenic infection of skin & subcutaneous tissues, usually arising in several contiguous hair follicles, with formation of connecting sinuses

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47
Q

What is the treatment for furuncles and carbuncles?

A
  • Moist heat
  • Systemic antibiotics with staph and G- coverage
    * PCN or Cephalosporin (Keflex or augmentin ) + MRSA coverage: Bactrim, Doxycycline or clindamycin *BCD)
  • Incision and drainage
  • Use an antibiotic such as ciprofloxacin (Cipro) if a gram negative organism is suspected.
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48
Q

Abscess
* Can present with or without what?
* What is the treatment?
* What should you do to help for localized abscess?
* Avoid what?

A
  • Can be present with or without cellulitis
  • Only effective treatment for an abscess is incision & drainage!
  • Use moist heat to help abscess localize or “come to a head”
  • Avoid aggressive manipulation
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49
Q

What is this?

A

Abscess
* If near rectum, then general surgeron needed because of a fisula

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50
Q

What is the txt of abscess?

A
  • Hospitalize toxic appearing patients & those with underlying diseases impairing immunity
    * In extremities look for circumferential coverage or joint involvement
  • C/S blood & any abscess, open wound, or drainage
  • If etiologic agent is suggested by patient’s Hx, Rx. is directed at a specific pathogen or group of pathogens
  • In absence of specific etiology Rx. directed at gram +
    * IV oxacillin(2 g q 6h) or cefazolin(2 g q8h) until signs of systemic toxicity have resolved; PO Rx. is then given to complete a 2-week course
    * Nafcillin or Vancomycin if MRSA high possibility
    * Agents active against anaerobes & gram-negative rods in diabetics with foot ulcers complicated by cellulitis
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51
Q

What is the txt of abscess when absence of specific etiology rx. at gram +

A
  • IV oxacillin(2 g q 6h) or cefazolin(2 g q8h) until signs of systemic toxicity have resolved; PO Rx. is then given to complete a 2-week course
  • Nafcillin or Vancomycin if MRSA high possibility
  • Agents active against anaerobes & gram-negative rods in diabetics with foot ulcers complicated by cellulitis
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52
Q

What are the different DDX of cellulitis?

A
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53
Q

Clostridial Cellulitis:
* What is this?
* Local extension where?
* Marked by what?

A
  • Gassy crepitant infection involving necrotic tissue with intact, healthy muscle spared (unlike in clostridial myonecrosis)
  • Local extension along fascial planes
  • Marked toxemia absent; Systemic effects mild
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54
Q

Clostridial Cellulitis:
* Sudden for gradual onset? What is the incubation period?
* Skin?
* Little to no what?
* What is the predominant organisms?

A
  • Gradual onset; incubation period 3 to 5 days
  • Skin rarely discolored
  • Little or no edema distinguishes from gas gangrene
  • Predominant organisms proteolytic & nontoxigenic clostridia, such as Clostridial sporogenes & Clostridium tertium
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55
Q

What is Dry Gangrene?

A

Dry gangrene of toes showing areas of total tissue death, appearing as black & lighter shades of discoloration of skin demarcating areas of impending gangrene

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56
Q

What is this?

A

Dry Gangrene- no drainage
* deeper-> death of bone and muscle
* Diabetes
* PAD-> smoking

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57
Q

Dry Gangrene:
* What is it the result of?
* Obtain what?
* What may complicate this condition?

A
  • Result of vascular disease
  • Obtain radiographs to help R/O clostridial myonecrosis & osteomyelitis-> x-ray or MRI, CT angiogram with runoff to see constriction
  • Soft-tissue infection may complicate this condition
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58
Q

What are the DDX of dry gangrene?

A
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59
Q

Necrotizing Fasciitis (NF):
* What type of infection?
* What is it characterized by?
* What is it?

A
  • Rare, rapidly progressive, life-threatening infection
  • Characterized by severe systemic toxicity
  • Necrosis of skin, subcutaneous tissue & deep & superficial fascia with sparing of underlying muscle
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60
Q

Necrotizing Fasciitis (NF):
* Disease is what?
* One of a group of clinical entities presenting as what?
* Previously described as what?

A
  • Disease is a clinical entity & not a specific bacterial infection
  • One of a group of clinical entities presenting as gangrenous or crepitant cellulitis
  • Previously described as hemolytic or acute streptococcal gangrene, gangrenous or necrotizing erysipelas, suppurative fasciitis & hospital gangrene
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61
Q

What are the 3 most important types of NF?

A
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62
Q

What are the prediposing conditions of NF

A
  • Majority of cases have occurred outside hospital following minor trauma such
    as abrasions, cuts, bruises, boils, & insect bites on extremities
  • May occur following surgical procedures
  • Rarely no apparent inciting injury
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63
Q

NF
* What does it follow?
* Massive necrosis of what? What follows that?
* What does pyrogenic exotoxin induce?

A
  • Following an insult, bacteria seed SC tissue & spread rapidly to adjacent tissue.
  • Massive necrosis of SC fat & fascia quickly follow due to elaboration of enzymatic toxins
  • Pyrogenic exotoxin induces mononuclear cells to synthesize TNF, interleukin-1 & interleukin-6 producing fever, shock, tissue injury, cytotoxicity & immunosuppression of B-lymphocyte function.
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64
Q

What are the early clinical findings of NF?

A
  • With destruction of vascular supply, overlying skin becomes necrotic & bulla form.
  • Destruction of cutaneous nerves results in total anesthesia over affected area
  • Involved skin is pale red without distinct borders & with blisters or bullae (pale to red)
  • Clue to Dx is pain & presence of SC swelling, particularly in absence of cellulitis
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65
Q

What are the late clinical findings of NF?

A
  • Minimal erythema & swelling
  • Involved skin is pale red without distinct borders & with blisters or bullae
  • Pale red areas progress to a distinct purple
  • Rapid progression of tenderness out of proportion to clinical appearance of wound
  • Systemic manifestation frequently out of proportion to local findings

Amputation

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66
Q

What is this?

A

Necrotizing Fasciitis -Late Clinical Findings
* Non blenching sign
* Bulla formation

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67
Q

What is this?

A

Scrotal Necrotizing Fasciitis -Late Clinical Findings
* Note the gas formation

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68
Q

What are the systemic manifestations of NF?

A
  • ARF (acute renal failure)
  • HF
  • Respiratory failure
  • Hypocalcemia
  • Hypotension
  • Toxic shock-like syndrome
  • Patients rapidly deteriorate
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69
Q

What are the signs of untreated NF?

A
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70
Q

What are the risk factors assoicated with NF?

A
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71
Q

NF treatment :
* What is the initally txt?
* What is used for GAS?
* What do you use for polymicrobial infection?

A
  • Initially target typical etiology with broad-spectrum coverage
    * Vancomycin + Pipercacillin/tazobactam + Metronidazole
  • For group A streptococci & clostridia, data suggest clindamycin may be superior
  • When polymicrobial infection suspected, therapy consists of metronidazole +ampicillin + gentamicin
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72
Q

Txt of NF
* What do you need agressive txt of?
* What might be useful in clostridial disease?

A
  • Aggressive management of septic shock & early surgical debridement essential to improved clinical outcome
  • Hyperbaric oxygen therapy may be useful in clostridial disease
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73
Q

What are the prognosis of NF? (5)

A
  • 20 to 50 % mortality rate
  • 3 or more risk factors increases mortality to 50%.
  • Survival related to timing of surgical intervention
  • Older the patient is & more coexisting diseases there are, higher mortality
  • Best outcomes associated with surgery in first 24 to 48 hours of the illness
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74
Q

Pyomyositis:
* What is it? What bacteria causes it?
* Where are most cases?
* What may antedate the onset of symptoms?

A
  • Deep infection of muscle usually caused by S. aureus & occasionally by group A Beta-hemolytic streptococci or enteric bacilli
  • Most cases occur in warm or tropical regions, & most occur among children
  • Nonpenetrating trauma may antedate the onset of symptoms
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75
Q

Pyomyositis:
* What do patients present with?
* Skin involvement?
* What might happen in older patients?
* Dx is made by what?

A
  • Patients present with fever & tender swelling of muscle
  • Skin is uninvolved or minimally involved
  • In older patients, myositis may mimic phlebitis
  • Dx. made by needle aspiration, US or CT scan
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76
Q

Clostridial Myonecrosis:
* Rapid spreading infection known as what?
* contaminated with what?
* What type of wounds are involved?
* Most likely to develop in wounds in which there has been what?
* Associated impaired arterial supply to limb or muscle group & gross contamination of wound by what?

A
  • Rapid spreading infection known as Gas Gangrene
  • Occurs in association with severe wounds of large muscle masses that have become contaminated with C.perfringens
  • Wounds commonly caused by high-velocity missiles of modern warfare & by accidental trauma
  • Most likely to develop in wounds in which there has been extensive laceration or devitalization of thick muscle masses, such as buttock, thigh, & shoulder
  • by soil, clothing, & other foreign bodie

Arterual involvement =rapid tissue death

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77
Q

Clinical Course of clostridial myonecrosis:
* Within how many days of injury? What happens?
* how is the patient?
* Skin?
* What are other complications?

A
  • Within 1 or 2 days of injury ,involved extremity becomes painful & begins to swell
  • Patient toxic & often delirious
  • Skin may appear uninvolved at first but eventually may develop a bronze-blue discoloration (sweet smell of discharge)
  • Hypotension, hemolytic anemia, & ARF complications
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78
Q

What is the txt of Clostridial Myonecrosis

A
  • Emergency surgery with wide debridement
  • Large doses of penicillin plus clindamycin may prevent further spread of bacilli

MY PC

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79
Q

Strep infection: pharyngitis
* What are general considerations?
* What are clinical findings?
* What are the labs and diganostics?
* What are complications?
* What are the DDX?
* What is the treatment?
* What is other things?

A
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80
Q

Strep infection: scarlet fever
* What are general considerations?
* What are clinical findings?
* What are the labs and diganostics?
* What are complications?
* What are the DDX?
* What is the treatment?
* What is other things?

A
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81
Q

Strep infection: Rheumaticfever
* What are general considerations?
* What are complications?
* What is the treatment?

A
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82
Q

What are these?

A
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83
Q

Non-group A strep infections
* What does GBS cause?
* What does it require?
* What is recommended in pregnancy?
* What is GBS apart of normally? what mean it cause?

A
  • GBS-sepsis, bacteremia, meningitis (in neonates)
  • Requires antepartum screening to identify carriers
  • Peripartum antimicrobial prophylaxis is recommended in pregnancy
  • GBS is part of normal vaginal flora, may cause septic abortion, endometritis, or peripartum infections and, less commonly, cellulitis, bacteremia, and endocarditis in adults
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84
Q
  • What is the txt of GBS?
  • What is the normal oral flora bacteria? What may they cause?
  • What does group D strep include? what does it cause? What do you tx it with?
A
  • Treatment: PCN or Vancomycin +/- gentamicin (2/2 in vitro synergism)
  • Viridans streptococci are part of the normal oral flora. Although these strains may produce focal pyogenic infection, they are most notable as the 2nd most common cause of native valve endocarditis.
  • Group D streptococci includeStreptococcus gallolyticus (bovis)and the enterococci.S gallolyticus (bovis)is a cause of endocarditis in association with bowel neoplasia or cirrhosis and is treated like viridans streptococci.->Tx: PCN G or Ceftriaxone or Vanc alone
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85
Q

Acute Rheumatic fever:
* What type of disease is ti?
* When does it preced onset?
* What does it cause?

A
  • Inflammatory disease, multi-systemic
  • Group A strep infection precedes onset by 2-6 weeks
  • Causes inflammation in the heart, joints, skin and central nervous system
    * Up to 60% of patients with Acute rheumatic fever progress to rheumatoid heart disease
  • Migratory joint pain, fatigue, fever, heart murmur, flat rash, chorea (Sydenham) and unusual behavior
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86
Q

What is the prevention, complication and txt of acute rheumatic fever?

A
  • Prevention – treat strep correctly
  • Complications - heart valve disease
  • Treatment – PCN-G x 1 or oral PCNs (pen+ amox but allergic use zpack)
    * ASA (fever, arthralgias, arthritis)
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87
Q

What is sydenham’s chorea? What causes it?

A

Hand does not relax
* Childhood complication of group A strep pharyngitis
* Usually self-limited
* One of the major Jones criteria for dx of acute rheumatic fever

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88
Q

what is the diagnosis criteria for rheumatic fever?

A
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89
Q

What are the recommended tests for possible acute rheumatic fever? (low yield because he did not talk about it?

A
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90
Q

What is the txt of Rheumatic fever?

A

PCN G 1.2 million units (THIS IS IV)
* Alt: Amoxicillin or PCN VK (THIS IS ORAL) or Cephalosporins or Macrolides or Clindamycin
* Chose based on allergy profile

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91
Q

Treatment of Rheumatic Fever:
* What do you manage arthritis with?
* What do you manage carditis with?
* What do you manage chore with

A
  • Arthritis management with NSAIDs
  • Carditis Management with conventional management of heart failure
    * Weak evidence of usefulness of IVIG, NSAIDs or glucocorticoids (does not prevent HF)
  • Chore management:Carbamazepine or valproic acid (this is seizure meds)
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92
Q

Endocarditis:
What is it?
What are the most common cause?

A
  • Endocarditis is a bacterial or fungal infection of the valvular or endocardial surface of the heart.
  • Etiology
    * Underlying valve disease (~50% of cases)
    * IVDA
    * Prosthetic valve
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93
Q

Endocarditis :
* What is the clinical presentation?
* What is the initating event in native endocarditis?
* When is transient bacteremia common?
* What is also a portal of access of microorganisms?

A
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94
Q

What are the common pathogens for native valve endocarditis?
* Who is it more common it (age and gender)

A

Etiology (typical):
* MCC=S. aureus (was previously streptococcal species)
* Strep viridans
* Enterococci
* HACEK organisms (1.4-3.0% of cases)
* Males > females
* Most: Age > 50; not common in kids

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95
Q

What are the common pathogens for injection drug user endocarditis? (right sided IE)
* What valve is mc affected?
* Who is it more common it (age and gender)

A
  • MCC=S. aureus
  • Enterococci
  • Streptococci
  • Fungi
  • Multiple organisms common
  • MC valve affected = Tricuspid (80-90%)
  • Septic pulmonary emboli w/ tricuspid infection
  • Young males common
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96
Q

What is pathogen is the notable cause of culture-negative endocarditis

A

Bartonella quintana

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97
Q

Prosthetic Valve
* What pathogen is early and late infection?

A

If early infection (w/in 2 mo. post-implantation)
* MCC-Staph (Gram + and Gram -) or fungi

If late infection (>2 mo. Post-implantation)
* MCC-Strep viridans

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98
Q

Left-Sided IE (MOST COMMON 80-90%)
* What are the risk factors?
* What valves are involved?
* What can the common sxs and signs?
* common associations with what?

A
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99
Q

Right-Sided IE (Isolated; ~10% of all IE cases)
* What are the risk factors?
* What is the MCC pathogen? What is the common assication?
* What are the common sxs?
* What are uncommon associations?

A
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100
Q

What is this?

A
  • Right side: pneumonia
  • Left: air/fluid lvl
  • From endocarditis that spread pass the heart
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101
Q

Clincial presentation of endocarditis (pass heart?)
* What are the sx?

A
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102
Q

What are classic skin and eye findings of endocarditis?

A
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103
Q

Approach to assessment of endocarditis
* Patients with IE should receive what?

A

Patients with IE should receive multidisciplinary care by infectious disease, cardiology, and cardiac surgery

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104
Q

Management of IE includes the following components:
* Prompt diagnosis and institution of effective antimicrobial therapy to reduce the risk of what?
* Neither anticoagulant therapy nor antiplatelet therapy is indicated to reduce what?
* Assessment of what?
* Identification of patients with an indication for what?
* how do you prevent the recurrent IE?

A
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105
Q

What labs do you need to get for endocarditis?

A
  • Blood cultures x 3 BEFORE starting antibiotics
  • CBC
  • CMP
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106
Q

What imaging is needed for endocarditis?

A
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107
Q

What is the modified duke criteria for endocarditis? (major and minor)

A
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108
Q

Txt plan for endocarditis
* Admit pt?
* What does most patient get?
* What does native valve IE get?
* What does Prosthetic valve IE?

A
  • Hospitalization, ID consult
  • Most get Vancomycin and Cefazolin and then adjust based on culture
  • Native Valve IE-> Vancomycin for 4-6 weeks
  • Typically left-sided unless caused by IVDA
  • Prosthetic Valve IE-> Surgical replacement +/- abx for 6 weeks
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109
Q

Txt plan of endocarditis:
* Txt of IE in IVDA?
* What is the surgical management?

A
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110
Q

What are the HACEK organisms?

A

HACEK organisms—A number of fastidious gram-negative bacilli are grouped by the acronym “HACEK” – these include:
* Haemophilus aphrophilus(subsequently called Aggregatibacter aphrophilus and Aggregatibacter paraphrophilus)
* Actinobacillus actinomycetemcomitans(subsequently calledAggregatibacter actinomycetemcomitans)
* Cardiobacterium hominis
* Eikenella corrodens
* Kingella kingae

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111
Q
  • HACEK organisms are isolated readily when?
  • What are they resistant to? What should not be used and what should be used for txt?
  • Virtually all HACEK organisms are highly susceptible to what drugs?
A
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112
Q

Who is endocarditis prophylaxis recommended for?

A
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113
Q

When is bacterial endocarditis prophylaxis recommended and not recommended?

A
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114
Q

AHA Guidelines for abx prophylaxis for IE updated in 2007?

A
  • Somewhat controversial b/c prophylaxis now recommended for fewer patients
  • Abx solely for GI or GU procedures are NOT recommended
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115
Q

ENDOCARDITIS

A
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116
Q

A
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117
Q

Clinical response to initial therapy:
* Most with IE become afebrile when?
* Patients withS. aureusendocarditis may respond how?
* What about Patients with right-sided endocarditis and septic pulmonary emboli?
* The initial microbiologic response to therapy should be assessed how?
* Serial physical examinations should be performed to evaluate for signs of what? Patients who develop new complications while on appropriate antimicrobial therapy (such as new emboli, heart failure, heart block, or other complications) should have what?
* How long does abx therapy last?

A
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118
Q

Meningitis:
* What is bacterial, viral and fungal meningitis?

A
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119
Q

What is the mc pathogen of bacterial meningits?

A

Streptococcus pneumoniae(~50%)-MCC

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120
Q

Bacterial meningitis

Neisseria meningitidis(~25%)
* Decreased dt what?
* Is the causative organism of what?

GBS:
* common in who?

listeria monocytogenes
* Common in who?

Haemophilus influenzaetype b
* common in who?

A
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121
Q

What are the predisposing Risk Factors of pneumococcal meningitis

A
  • Pneumococcal PNA
  • Sinusitis
  • Otitis media
  • Alcoholism
  • Diabetes
  • Splenectomy
  • Hypogammaglobulinemia
  • Complement deficiency
  • Head trauma w/ basilar skull fracture & CSF rhinorrhea
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122
Q

Clinical Presentation of bacterial menginitis
* Most present with sx when?
* What is the class clinical triad? Triad will not always be present BUT what will be?

A
  • Acute fulminant illness vs. subacute infection
  • Most present within 24hrs of symptoms onset
  • Class clinical triad: fever, headache and nuchal rigidity (“Stiff neck”) -> Pathognomonic, but is a late sign
  • Triad not always present BUT fever, and either headache, stiff neck, or AMS will be present in nearly 100% of pts w/ bacterial meningitis
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123
Q

Clinical Presentation of bacterial menginitis
* What are the other symptoms and what tests can be done?

A
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124
Q

What are the labs/rads that need to be done for bacterial meningitis?

A
  • Blood cultures
  • CT/MRI before LP -> not everyone needs imaging before LP. Only of GCS is reduced (<12) or there is evidence of brain “shift” on physical exam
  • LP with CSF analysis
  • Other labs to consider:
    * CBC
    * CRP
    * Lactic acid
    * Lactate dehydrogenase
    * HIV
    * Procalcitonin
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125
Q

What is the CSF results in bacterial meningitis?

A
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126
Q

What are the DDX of bacterial meningitis?

A
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127
Q

What is the txt of and process of bacterial meningitis?

A
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128
Q

What is the empiric txt of bacterial meningitis

A
  • Dexamethasone + 3rd or 4th cephalosporin (Ceftriaxone, Cefotaxime)
  • And Vancomycin PLUS Acyclovir
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129
Q
A
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130
Q

Dexamethasone controversy for bacterial meningitis
* The efficacy ofdexamethasonetherapy in preventing what?
* What did Three large randomized trials in low-income countries (sub-Saharan Africa, Southeast Asia) show?
* The lack of efficacy ofdexamethasonein these trials has been attributed to what?
* The results of these clinical trials suggests what?

A
  • The efficacy ofdexamethasonetherapy in preventing neurologic sequelae is different between high- and low-income countries.
  • Three large randomized trials in low-income countries (sub-Saharan Africa, Southeast Asia) failed to show benefit in subgroups of patients.
  • The lack of efficacy ofdexamethasonein these trials has been attributed to late presentation to the hospital with more advanced disease, antibiotic pretreatment, malnutrition, infection with HIV, and treatment of patients with probable, but not microbiologically proven, bacterial meningitis.
  • The results of these clinical trials suggest that patients in sub-Saharan Africa and those in low-income countries with negative CSF Gram’s stain and culture should not be treated withdexamethasone.
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131
Q

Adjunctive steroids are effective in reducing inflammation and improving clinical outcomes in some causes of meningitis such as: (4)

A
  • S. pneumoniae (mortality)
  • H. influenzae (hearing loss)
  • N. meningitidis (arthritis)
  • M. tuberculosis (mortality)
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132
Q
  • Steroids are detrimental in what bacterial meningitis?
  • Use in viral encephalitis is what?
A
  • Steroids are detrimental in Listeria or Cryptococcus
  • Use in viral encephalitis is unclear (limited studies)
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133
Q

Mortality (ranges 5-25%) of bacterial meningitis increases when (6)

A

(1) Decreased level of consciousness on admission
(2) Onset of seizures within 24h of admission (33%)
* 3% remain with seizure d/o after recovery

(3) Signs of increased ICP
(4) Young age (infancy) and age >50
(5) Presence of comorbid conditions including shock and/or the need for mechanical ventilation
(6) Delay in the initiation of treatment (esp with imaging prior to LP)

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134
Q

What are the clinical signs and sxs of viral meningitis

A
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135
Q

What are the labs for viral meningitis

A
  • CSF: Normal glucose, normal or elevated opening pressure, normal or slightly elevated protein
  • CBC w/ diff
  • CMP
  • CRP
  • CK
  • Lipase
  • HIV
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136
Q

What are the rad for viral meningitis

A

Rads: MRI preferable to CT; neither absolutely necessary if uncomplicated viral meningitis
* Unless there are risk factors
* HSV-1 prefers temporal lobe involvement

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137
Q

Most common and less common Viruses Causing Acute Meningitis in North America

A
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138
Q
  • What are the DDX of viral meningitis?
  • What is the txt?
A
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139
Q

Encephalitis from viral meningitis
* patients persent with what?
* What is the mmc and what is more common in encephalitis?
* By contrast, patients with aseptic meningitis most commonly present with what?
* Patients with features of both may be considered to have what?

A

NEED A CT BECAUSE VIRAL

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140
Q

Subacute meningitis (fungal or atypical bacterial)
* What are the clinical sxs?
* What are the labs?

A
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141
Q

Fill in the txt for the subacute meningitis

A
142
Q

What is highly suspicious for tuberculous meningitis?

A

The combination of unrelenting headache, stiff neck, fatigue, night sweats, & fever with a CSF lymphocytic pleocytosis and a mildly decreased glucose concentration is highly suspicious for tuberculous meningitis.

143
Q

Pearls of meningitis
* What are signs?
* Skin?
* What are characterisitc but late signs?
* Purulent spinal fluid with what?
* What confirms the diagnosis?
* What does bacterial meningitis have?

A
  • Fever, headache, vomiting, delirium, convulsions.
  • Petechial rash on skin and mucous membranes in many.
  • Neck and back stiffness and positive Kernig and Brudzinski signs are characteristic, but are usually late signs.
  • Purulent spinal fluid with gram-negative intracellular and extracellular diplococci.
  • Culture of cerebrospinal fluid, blood, or petechial aspiration confirms the diagnosis.
  • Bacterial meningitis CSF: High neutrophils, Low glucose, High protein, Increased opening pressure (>180mmH20)
144
Q

Pearls of meningitis
* What does viral CSF profile show?
* What is prodominace in viral CSF?
* Subacute/fungal CSF findings?
* What is required for confirmation?

A
  • Viral CSF Profile: Normal glucose, lymphocytic pleocytosis, negative Gram stain
    * Red blood cells predominance in the absence of traumatic tap is suggestive of HSV (or other necrotizing encephalitides)
  • Subacute/fungal: Glucose is usually lower than in acute bacterial meningitis (which is already low)
  • PCR is required for confirmation

Pleocytosis: It is oftendefinedspecifically as an increased white blood cell count incerebrospinal fluid.

145
Q

Community-acquired Pneumonia (CAP)
* Occurs when?
* What is the typical or atypical presentation?
* What the MC bacterial pathogen?

A
146
Q

Nosocomial (VAP +/- MDR & HAP)
* When does it happen?
* What are the MC pathogens?
* _ pathogens?

A
  • Occurs during hospitalization after first 72 hours
  • MC bacterial pathogens are gram-negative rods (E. coli, Pseudomonas) and Staphylococcus aureus
  • MDR Pathogens
147
Q

What are two ways of prevention of pneumonia?

A
  • Influenza vaccine (yearly)
  • Pneumococcal vaccine (>65 years and any high-risk any patients) High risk: [heart disease, sickle cell, pulmonary disease, diabetes, alcoholic cirrhosis or asplenic individuals]
148
Q

Microbiology of CAP:
* What are the typical and atypical pathogens?

A
149
Q

Microbiology of HAP
* What are the pathogens that are the MCC of HAP?
* Nearly half of HAP cases are what?
* In patients receiving mechanical ventilation, what pathogens are important?

A
150
Q
A
151
Q

What are the complications of pneumonia

A
152
Q

Diagnostic approach to CAP- What are the PE findings?

A
153
Q

Diagnostic approach to CAP- What are the lab studies

A
  • Pulse oximetry (RA with rest & activity) ⭐️
  • CBC
  • CMP
  • ABGs
  • Sputum gram stain/cultures
  • Blood cultures
  • Urine for Legionella antigen
  • Procalcitonin

⭐️ admit or go home based on this: over 88 on 6 min walk test then they are good

154
Q

What is the imaging of cap?

A

cxr

155
Q

What does this show?

A
156
Q
A
157
Q

What are the DDx of pneumonia

A
158
Q

What is the outpatient txt of CAP? (no psedomonas or MRSA, high risk mycoplasma and high risk for MRSA)

A
159
Q

What is the treatment of CAP for inpatient?

A
160
Q

Rocky Mountain Spotted Fever
* What is the cause
* What is the transmission?
* Typically occues when?
* When are common months?
* Where does it attaches and attacks?

A
161
Q

RMSF:
* What is the incubation period?
* What are the acute onset of sym?
* Rash?
* Involves what?
* What may occur?

A
  • Incubation period 2-14 days
  • Acute onset of high fever, chills, headache, nausea, and vomiting, myalgias, restlessness, insomnia, irritability
  • The rash appears between day 2 and 6 of the fever – initially wrists, ankles and spreads centrally to arms, legs and trunk over next few days (~10% have no rash)
  • Involves palms and soles
  • Hard palate lesions, facial flushing, conjunctival injection may occur
  • Splenomegaly, hepatomegaly, jaundice, ARDS and necrotizing vasculitis may occur
162
Q

What are the skin findings in RMSF?

A
163
Q

Neurologic Findings of RMSF
* Focal neurological defects may be present including what?
* What are symptoms?
* CSF contains what?
*

A
164
Q

RMSF
* What are the lab findings?
* What is diagnosis made during acute phase?

A
  • Thrombocytopenia, hyponatremia, elevated aminotransferases, hyperbilirubinemia – common
  • Diagnosis during acute phase can be made by immuno-histology or PCR demonstration
165
Q
  • What is challenging about RMSF?
  • What do you need to rule out?
A
  • Challenging – rarely is the triad of fever, rash and tick bite present – most patients will not know they were bit by a tick
  • Must rule out meningococcemia
166
Q

What is the txt and prevention of RMSF?
What is not recommended?

A
167
Q

Lyme borrlisosis
* What is the pathogen?
* What is the vector?
* What are the major areas?
* When does disease peak (seasons)?

A
  • Borrelia burgdorferi, a fastidious spirochete
  • Principal vector in these regions is deer tick (Ixodes scapularis) & > 20% of these ticks are infected with B. burgdorferi
  • Major areas of disease NE, Wisconsin & Minnesota in Midwest
  • Incidence of disease peaks during summer
168
Q

Alt: Deer tick (Ixodes scapularis) feeding
* What might is cause and what does this mean?
* Transmission of B. burgdorferi usually occurs only after what?

A
169
Q

Stage one of lyme
* What is the incubation period?
* What is the skin issue?

A

An expanding erythematous rash not associated with scaling is characteristic of erythema chronicum migrans. Disease first appears weeks to months after a tick bite. Lesion begins as a red macule at the site of the bite;

170
Q

Stage 2 of lyme
* Within days of onset of what?
* Skin?
* Frequently accompanied by what?
* Symptoms usually resolve when

A
171
Q

Stage 2 of lyme
* Cardiac issues?
* What other pain is present?

A
172
Q

Stage 2 lyme
* After several weeks/months, ~15% develop what?
* CSF shows what?
* Early neurologic abnormalities resolve when

A
173
Q

stage 3 lyme
* When should this happen? What are the symptoms?

A
174
Q

Lyme disease
* Recognition of a characteristic clinical picture with what?
* What is the standard tool
* Several weeks after infection most pts develop what? What is this detected by?
* IgM and IgG-specific assays are recommended when?
* Persistence of serologic positivity in who?

A
175
Q

Botulism:
* What is it and what is caused by?
* What is the pathophysiology?
* feared as?

A
  • Paralytic disease caused by botulinum toxin produced by Clostridium botulinum
  • Pathophysiology – blocks release of neurotransmitter acetylcholine at neuromuscular junction
  • Extremely potent, feared as a possible bioterrorism agent
176
Q

What are the 3 naturally occurring forms of botulism?

A
  • Food borne – home canned foods, smoked meats, vacuum packed fish
  • Infant – ingestion of honey
  • Wound – injection drug use
177
Q

Clinical Presentation of botulism
* 12-36 hours after ingestion ?
* What are other s/s?
* What usually causes death?

A
178
Q

Botulism:
* Clinical dx by what?
* Once suspected – contact who and do what?
* Ideally what should be administered and when?
* When should treatment start?
* What are other DDX?

A
179
Q

Botulism Treatment
* What is the cornerstone tx? What are the two types?
* Antibiotics typically not given for what?
* What do you give for Wound botulism

A
180
Q

Tetanus:
* What pathogen causes this?
* What does it caue?
* What are the initial sxs?
* What is diagnosis process?

A
  • Clostridium tetani is anaerobe ubiquitous in soil, but can exist intact for years on other surfaces
  • Infection in humans; causes syndrome of muscle spasms and pain in trunk, jaw, and neck, respiratory distress or arrest
  • Initial Sxs: Trismus (lockjaw), muscle pain and stiffness, back pain, and difficulty swallowing, then risus sardonicus
  • Diagnosis: Clinical, Culture ofC. tetanifrom a wound provides supportive evidence
181
Q

What are the different preventions and given after a possible tetanus situation? (give ages)

A

DTaP
* diphtheria, tetanus, and pertussis vaccine for kids under age 7 (2mo, 4mo, 6mo, 15-18 mo, 4-6 years, DT for those with pertussis susceptibility

Tdap
* for ages 11 thru 64 who have never yet had a dose, but Td should be use if Tdap is not available or if they have already had one dose of Tdap

Td (Adacel)-> in emergency room
* pts over age 7, preferable than just tetanus alone as many adults susceptible to diphtheria, booster every 10 years

TIG (human or equine) human preferred to eliminate potential for hypersensitivity reaction to equine

182
Q

When do people get the series of tetanus? When do you get booster?
* Tetanus immunization in pregnanacy?

A
183
Q

What do you give or not give with a patient with a clean, minor wound? (one with unknown or less than 3 doses and if they had more than 3 does then another)

A
  • patient is unknown or less than 3 doses: give TdaP
  • If Patient has 3 or more doses: do not give TdaP if less than 10 years
  • If patient is unknown or under 3 doses and does not have 3 or more doses: do not give TIG with +/- TdAP
184
Q

What do you give or not give with a patient with a dirty wound? (one with unknown or less than 3 doses and if they had more than 3 does then another)

A
  • Unknown or less than 3 doses: give Tdap
  • 3 or more doses: do not give TdaP if less than 5 years
  • If unknown or less than 3 doses: give TIG with -/+ TdaP
  • If has 3 or more doses: then do not give TIG
185
Q

What are the tetanus prone wounds?

A
186
Q

What are the non-tetanus prone wounds?

A
187
Q

What are the DDX of tetanus?

A
188
Q

Symptomatic Treatment of tetanus:
* What do you need to do with the wound?
* What is preferred (pharm)?
* What may exacerbate spasms and in one study was associated with increased mortality?
* What do you need to administer early?
* What is the preparation of choice?

A
  • Clean and debride wound of necrotic material in order to remove anaerobic foci of infection and prevent further toxin production
  • Metronidazole (400 mg rectally or 500 mg IV every 6 h for 7 days) is preferred-> Alt: PCN G or Doxycyline
  • Penicillin (100,000–200,000 IU/kg per day) may exacerbate spasms and in one study was associated with increased mortality.
  • Administer Antitoxin (early): Human tetanus immune globulin (TIG)-PREFERRED OR equine antitoxin
  • TIG is the preparation of choice, A single IM dose (3000–5000 IU) is given, with a portion injected around the wound.
189
Q

Tetanus:
* How do you treat/control the spasms?
* How do you tx cardiovascular instability?
* How long is recovery?

A
190
Q

Diphtheria:
* What pathogen causes diphtheria
* How does it spread?
* What is the most common form?
* What is the classic physical exam finding?

A
  • Corynebacterium Diphtheriae
  • Spread via respiratory secretions, produces an exotoxin responsible for myocarditis and neuropathy
  • Most common form – pharyngeal, but rare in the US thanks to DTaP/Tdap.
  • Classic physical exam finding – pseudomembrane covering tonsils and pharynx
191
Q

Diphtheria:
* What are other symptoms?
* What are the most common serious complications?
* What is the dx?

A
  • Symptoms – mild sore throat, fever, malaise
  • Pericarditis and neuropathy are the most common serious complications. Neuropathy usually involved the cranial nerves
  • Diagnosis – typically clinical, may culture
192
Q

Differential DX, Prevention and Treatment-> Diphtheria
* What do you need to rule out?
* What does Diphtheria require? (txt)
* What do you need to culture?

A
  • Rule out other etiologies for pharyngitis, neuropathy – but do not withhold treatment
  • Requires admission with emergent treatment – removal of membrane if causing airway obstruction, antitoxin and PCN G or erythromycin (to prevent transmission to susceptible contacts)
  • Isolate until 3 consecutive cultures are negative
193
Q

What are the diphtheria contacts treated with?

A

Treat contacts with Erythromycin

194
Q

What is this?

A
195
Q

What is this?

A
196
Q

Tuberculosis
* What is the cause?
* The most common what?
* At are high risk areas?

A
  • Cause – Mycobacterium tuberculosis, a small, slow growing aerobic bacilli
  • The most common mycobacterial infection
  • The leading infectious cause of morbidity and mortality in adults worldwide
  • In areas of world where both TB and HIV are prevalent, HIV/AIDS is the highest risk factor

  • One of the most widespread and deadly illnesses globally
  • ~10 million cases annually
  • 1.7 mil deaths in 2016
197
Q

What remains a health crisis for TB?

A

Multidrug-resistant TB (MDR-TB) remains a public health crisis and a health security threat. A global total of 206 030 people with multidrug- or rifampicin-resistant TB (MDR/RR-TB) were detected and notified in 2019, a 10% increase from 186 883 in 2018

198
Q

Primary Infection-TB
* Rarely causes what?
* What is the pathophysiology?-> what is the risk threshold?
* How is it spread during this stage?
* Rarely develops into what?
* People infected with TB bacteria have a lifetime risk of what?
* What population is at higher risk of falling ill?

A
  • Rarely causes acute illness, 95% asymptomatic.
  • Pathophysiology – M. tuberculosis bacilli must be ingested by alveolar macrophage, those not killed by macrophage, replicate and kill macrophage with help from CD8
    * possible risk threshold of 250 hours-> to actually get disease
  • Spread – usually not transmissible in primary stage
  • Rarely develops into acute illness with pneumonia, marked lymph node enlargement (mediastinal or hilar), pleural effusions.
  • People infected with TB bacteria have a 5–15% lifetime risk of falling ill with TB
  • Those with compromised immune systems, such as people living with HIV, malnutrition or diabetes, or people who use tobacco, have a higher risk of falling ill
199
Q

Latent Infection- TB
* When does it occur?
* What is the pathophysiology?
* What allows the bacilli to survive for years?
* What determines resoultion, dormancy and activation?
* What is positive during the latent phase?

A
200
Q

Active Disease of TB
* More commonly reactivates when?
* Where is the most common place for reactivation?
* What increase the likelihood of reactivation?
* Who has a risk?
* What does TB do?

A
201
Q

Active Pulmonary Tuberculosis:
* May not have what?
* Typically feel what?
* What is common?
* May have what?
* HIV presentation is atypical- how do they present?

A
202
Q

Diagnosis of TB
* What is the becoming a thing of the past, although still used?
* What is the gold TB test?
* What imaging?
* What culture?
* Test all +TB patients for what?
* What do you need for definitive diagnosis?

A
  • Tuberculin skin test is becoming a thing of the past, although still used
    * TB T-Spot test (most sensitive) or Quantiferon Gold TB test (blood test that detects memory t cells that produce IFN-γ in response to M. tuberculosis antigens, using the enzyme-linked immunospot technique.
  • Chest x-ray
  • Acid-fast stain and culture
  • Test all +TB patients for HIV, obtain baseline liver and renal function tests.
  • Must culture sputum for definitive diagnosis and to isolate bacteria for drug sensitivity
203
Q

What are the different reactions frome th TB skin test?

A
204
Q

Chest X-ray
* What do you see?
* What is shown on reactivation or primary infection?
* What may be TB or histoplasmosis?

A
205
Q

Treatment for Acute TB:
* What is the pharm for txt?
* What is the difference of intensive and continuation phase?

A
  • Isoniazid INH +Rifampin +Pyrazinamide +Ethambutol (RIPE)
  • Daily dosing for the first 2 months (intensive phase)
  • Daily dosing or three times per week (continuation phase)
206
Q

Treatment of Latent TB
* Patients with a positive PPD but normal CXR and otherwise no symptoms should receive what?

A
  • Three months of once weekly Isoniazid + rifapentine
  • Four months of daily rifampin
  • Three months of daily isoniazid + rifampin
207
Q

Atypical Mycobacteria/Nontuberculous Mycobacteria (NTM)
* How many species?
* Found in what?
* Typically cause what?
* What are the 4 clinical syndromes?

A
  • Approximately 200 NTM species
  • Found in fresh and salt water, soil, household dust
  • Typically cause chronic lung infections
  • 4 clinical syndromes – lung, lymphadenitis, cutaneous, disseminated
208
Q

Mycobacterium avium complex - MAC
* Who do you see with in?
* No what type of transmission?
* May be what?
* HIV might have what?
* What is the diagnoses?

A
  • Elderly and immunocompromised primary
    * Is AIDS defining illness, typically see CD4 counts <50
  • No known person to person transmission
  • Typically present as lung disease
  • May be cutaneous, lymphadenitis (children)
    * Scrofula means outside of the lung presentation
  • Disseminated infections in patients with HIV
  • Diagnoses – acid-fast stain and sample culture
209
Q

What is the txt of MAC?

A

Treatment – typically Azithromycin or Clarithromycin
* Alt: clarithromycin, ethambutol, rifabutin

MAC-AC for txt

210
Q

What is this?

A

Cutanous MAC

211
Q

What is this?

A

Lymphadenitis (scrofula) MAC

212
Q

Mycobacterium marinum:
Where is it found?
Enters via what?
What does it cause?
What is the txt?

A
  • Found in fresh and salt water
  • Enters via break in skin
  • Causes cutaneous lesions – begins as an erythematous blue/purple papule that typically ulcerates
  • DX – culture
  • TX – opinions vary – Clarithromycin
    * In superficial cutaneous infections minocycline, clarithromycin, doxycycline and trimethoprim-sulfamethoxazole as monotherapy are effective treatment options
213
Q

What is this and what do you treat it with?

A

Mycobacterium marinum
* TX – opinions vary – Clarithromycin
* In superficial cutaneous infections minocycline, clarithromycin, doxycycline and trimethoprim-sulfamethoxazole as monotherapy are effective treatment options

214
Q

Leprosy (Hansen’s Disease)
* What pathogen causes this/
* Rare or common?
* Passed by what?
* Who has natural immunity?

A
  • Mycobacterium leprae
  • Now rare - ~150 cases a year in US and 250,000 globally (CDC)
  • Passed by Armadillos
  • 95% of people have a natural immunity, risk highest in Africa, Asia
215
Q

What is the pathophysio of leprosy?

A

Attacks nerves, skin, mucous membranes - causes loss of sensation, can result in paralysis of hands and feet, body may reabsorb affected digits, causes corneal ulcers and blindness, “saddle-nose deformity” – due to nasal septum damage.

216
Q

How do you dx and tx leprosy?

A
  • DX – skin biopsy
    * FITE stain (acid fast)
    * Lepromin Skin test is alternative
    * May be negative in Lepromatous leprosy which carries high infectivity and neurological damage
  • TX – Dapsone, rifampicin, clofazimine
217
Q

What is this? What do you treat it with?

A

Leprosy
* Dapsone, rifampicin, clofazimine

218
Q

Legionella pneumophila
* What is the pathogen and where it grows?
* Who has a higher incidence of occurrence
* What are the sxs?

A
  • G- bacilli colonizing water supply (infects amoebas and resists Cl and temperature)
  • Older age, COPD and smoking have higher incidence of occurrence
  • Sxs – high fever and nonproductive cough with GI Sxs, also HypoNa. Confusion is common. Bradycardia is profound. CXR shows consolidations.
    * Commonly occurs with diarrhea

air conditioner worker, fountain worker, cruise worker

219
Q

What is pontiac fever?

A

Legionella pneumophilia
* Pontiac Fever - headaches, fever, myalgias without pneumonia
* In epidemic regions via airborne transmission
* Less serious

220
Q

Legionella (Legionnaire’s Disease)
* What is the dx and tx?

A
  • Will not show on gram stain, order urine antigen test or sputum culture
  • Tx: Azithromycin or Levaquin or doxy
    * don’t respond to PCN and like or aminoglycosides
221
Q

Brucellosis
* What pathogen?
* Most common in what people?
* What are the typical viral symptoms? What are the rare symptoms?

A
  • Brucella melitensis
  • Most common in people handling meat or those ingesting contaminated milk or meat (cattle, goats, sheep, camels, dogs)
  • Typical viral symptoms: fever, chills, weakness, body aches
  • Rare symptoms: lumbar osteomyelitis, spondylitis, endocarditis, epidydimoorchitis
222
Q

Brucellosis
* How do you dx
* how do you tx?

A
  • Dx: titer for Brucella agglutinins or Culture, but culture may take 6 weeks
  • Tx – Doxycycline + Rifampin for 6 weeks. Repeat cultures should be made every 3-6 months for 2 years.
223
Q

Tularemia
* What pathogen?
* Transmitted from what?
* What are sxs?
* How do you dx?
* What is Ulceroglandular tularemia ?

A
  • Francisella tularensis
  • Transmitted from rabbits (rabbit brains)/ticks/or deerfly. Most common in AR/OK/Missouri.
  • Sxs – fever, chills, myalgias, headaches
  • Dx based on serologic agglutination tests (>1:160 is +)-> Doesn’t gram stain
  • Ulceroglandular tularemia (80%) – follows skin inoculation forming papule that develops into punched-out ulcer with necrosing base.
224
Q

What is the txt of tularemia?

A

Tx – DOC is streptomycin

225
Q

Plague:
* What is the pathogen?
* How it is transmitted by?
* What are the sxs?
* How do you Dx?
* What is the txt?

A
  • Yersinia pestis
  • Transmitted by bite of rodent flea or pigs mostly in Southwest US
  • Sxs – rapid onset of fever, myalgias and arthralgias, painful LAD – buboes (large lymphoditis). Can cause pneumonia
  • Dx – stains reveal bipolar safety-pins (CSF or blood or aspirated bubo)
  • Tx – DOC is streptomycin (Alt: tetracycline for pneumonia)->If not treated – death within 10 days due to DIC.
226
Q

Q Fever - Coxiellosis
* This is the common cause of what?
* What is this due to?
* What are the sx?
* How do you dx?
* What is available?

A
  • Common cause of FUO in chronic disease pattern
  • Due to Coxiella burnetti, which naturally infects goats, sheep and cattle. The bacteria is inhaled.
  • Sxs: typical viral – fever, chill, sweats, headache, muscle aches, vomiting, cough. May cause endocarditis and hepatitis
  • Dx: PCR or serology
  • Vaccine is available
227
Q

How do you txt q fever-coxiellosis? What about endocarditis?

A
  • Tx: Doxycycline for 2-3 weeks
  • Add hydroxychloroquine in endocarditis
228
Q

What are the eight Human Herpes Virus Infections Family?

A
  • HHV 1/2 - Herpes simplex virus (HSV) type 1, HSV type 2
  • HHV 3 - Varicella zoster virus (VZV) type 3
  • HHV 4 - Epstein-Barr virus (EBV), infectious mononucleosis – type 4
  • HHV 5 - Cytomegalovirus (CMV) – type 5
  • HHV 6/7 – Roseola or 6th disease and several syndromes
  • HHV 8 – Kaposi sarcoma (HIV), lymphoma
229
Q

Pathophysiology of viral infection
* Virus must contact how to infect?
* Where does the virus go in the body?
* What is latency?
* What increases the Likelihood of recurrences?

A
  • Virus must come in direct contact with either mucosal surface or abraded skin
  • Makes its way to the ganglion (nerve) via neural transmission
  • Latency – will be dormant until a stressor occurs
  • The more severe the primary infection (size and # of lesions) the more likely recurrences will occur
230
Q

HSV 1 and HSV 2:
* What are they?
* What are sxs?

A
231
Q

HSV sequela:
* What happens to the eyes?
* What happens to the CNS?
* When does disseminated infection happen?
* What is the cause of bell’s palsy?
* What happens to the esophagus
* What happens to the prostate?
* What happens to the skin?
* What happens to the liver?

A
232
Q

Varicella-Zoster Virus (HSV-3)-> Varicella:
* What is it?
* What happens to the skin?
* Typically occurs when?
* Contagious or not?
* What is the classic sign?

A
  • Chicken pox
  • Pruritic rash – starts on face and body – moves to extremities
  • Papules-vesicles-honey colored crust
  • Typically occurs in childhood
  • Very contagious – droplet or contact
  • Classic “dew drop on rose petal”
233
Q

Varicella-Zoster Virus (HSV-3)-> Zoster:
* What is it?
* What happens to the skin?
* What happens first?
* What age?
* How common?

A
  • Shingles
  • Painful rash
  • Tingling and pain first, erythematous based rash along a dermatome
  • Half of pts >60
  • 25% of adults in lifetime
  • Annual incidence – 1 mil in US
234
Q

What are these examples?

A
235
Q

Herpes Zoster (Shingles)
* HZ is reactivation of what?
* What is the skin issue?
* What is the incubation period?
* What is prodrome?

A
  • HSV covered previously
  • HZ is a reactivation of varicella
  • Eruption of grouped vesicles on an erythematous base usually limited to a single dermatome (“shingles”)
    * Incubation period of 10-16 days; initial viremia w/i 4-6 days disseminating to other organs (liver, spleen, sensory ganglia), second viremia 10-21 days with presentation of rash
    * Prodrome: coryza, myalgia, nausea, decreased appetite, HA -> rash, low grade fever, malaise, oral sores
236
Q

Herpes Zoster (Shingles)
* Where does the virus hide?
* What is the most common age?
* What can last months to years?

A
  • Virus “hides” in a dorsal spinal root until reactivated.
  • Most common in ages > 50
  • Postherpetic neuralgia, lasting months to years may occur, especially in elderly
237
Q

Herpes Zoster:
* What is the method of choice to dx?
* What is another ways to dx (smera, antibody, serologic, in utero)?

A

Method of choice: RT-PCR – swab fluid-filled vesicle, or may use crust

Tzank smear of both roof & floor of a herpetic vesicle demonstrating a multinucleated giant cell.
* Direct fluorescent antibody (DFA) – replaced Tzank smear (use Giemsa stain -> multinucleated giant cells)
* Serologic – weak, tests IgG (must be high); ELISA used for screening
* In utero: VZV DNA or presence of IgM in fetal blood/cord or amniotic fluid; US – limb deformities, microcephaly, hydrocephaly, IUGR

238
Q

What is this?

A

herpes zoster
* Tzank smear of both roof & floor of a herpetic vesicle demonstrating a multinucleated giant cell.

239
Q

What is this? How would you describe this?

A

Herpes Zoster
* This eruption consists of a dermatomal distribution of umbilicated vesicles on an erythematous base.
* Note occasional cluster of hemorrhagic vesicles.

Unilateral: do not cross midline

240
Q

What is the presentation of herpes zoster?

A
  • Erythema or tingling
  • Vesicles appear in a dermatomal pattern
  • Vesicles progress to pustules
  • Crusting occurs
  • Lesion disappear in 3 - 4 weeks
  • Much less contagious than chickenpox.
241
Q

What is this?

A

Ophthalmic Herpes Zoster
* This patient has vesicles in ophthalmic division of CN V bilaterally

242
Q

What is this?

A

Disseminated Herpes Zoster Infection
* Vesicles are seen over entire face, representing disseminated HZV infection (multiple dermatomal distributions)

243
Q

What is zoster treatment?

A
  • Acyclovir (Zovirax)
    * Higher doses required
    * 800 mg. 5 times a day for 7 - 10 days
  • Famciclovir (Famvir) 500mg. TID
  • Valacyclovir (Valtrex) 1g TID X 7
  • Zovirax cream ineffective for VZV
244
Q

Zoster Treatment
* What are other txts besides acyclovir, famciclovir, valacyclovir?

A
  • Domeboro soaks
  • Analgesics
  • Post herpetic neuralgia
    * Nerve blocks (lidocaine)
    * Capsaicin (Zostirx)
    * Antidepressants (pain and wellbeing)
  • VZV IVIG (immunoglobulin) for immunocompromised
  • Vaccination
245
Q

Zoster Complications in adults, in utero and other?

A
  • Adults: more severe disease, Pneumonia
  • In utero: Varicella congenital syndrome- hypoplasia of GI/GU tract and extremities, cortical atrophy, chorioretinitis, microcephaly, low birth weight. Chickenpox at birth
  • Secondary bacterial infections, CNS involvement, myelitis, GBS, meningitis
246
Q

Epstein-Barr Virus
* What is the infection?
* Maybe asymptomatic but what are the systemic manifestions?
*

A
  • HHV4 infection – Causes Mononucleosis
  • Maybe asymptomatic
    * Systemic manifestations: FATIGUE, fever, malaise, HA, sore throat with exudates, LAD?, splenomegaly, lymphocytosis, abnormal LFTs
    * Fatigue and pharyngitis can linger for 6+ months and may recur with compromised immune system
247
Q

Epstein-Barr Virus
* How do you dx?
* What is the tx?

A

Dx: Serologic testing
* Atypical lymphocytosis on peripheral smear
* Heterophile Ab testing (Rapid Mono-Spot test-> blood test) * (kids may not produce so low sensitivity)
* Viral capsid Ag for confirmation : IgM = acute infection, IgG = chronic or prior infection
* In absence of testing ability, prophylactic amoxicillin may serve as diagnostic tool

Tx: Supportive
* Avoid contact sports dt splenomeganly
* Recent studies show 40 fold increased risk of MS development

248
Q

CMV:
* What virus is it?
* May be asymptomatic in who?
* What are the sx of Reactivation 2◦ immunosuppression?
* What is seen in severe immunocompromised host?

A
  • HSV 5 – reactivates in compromised immune system
  • Maybe asymptomatic in immunocompetent host
  • Reactivation 2◦ immunosuppression: fatigue, low grade fever, chills, sweats, myalgia, decreased appetite, LAD, sore throat, HA, rash, leukocytosis, anemia, abnormal LFTs, +Rf, +ANA (CD4<50)
  • In severe immunocompromised hosts: hepatitis, pneumonitis, colitis, retinitis, encephalitis, myelitis
249
Q

CMV
* How do you dx?
* What is the tx?

A

Dx: Gold standard – Inclusions on Histology with + immunochemistry
* Preferred – Quantitative PCR – detects viral DNA in sample OR
* Serology – detects CMV IgM antibodies - indicates acute infection

Tx: Immunocompromised only (ganciclovir, foscarnet, cidofovir, valganciclovir)
* Seronegative transplant patients should receive prophylactically

250
Q

Roseola Infantum
* What is the virus? Where does it replicate?
* What are the sxs? what are Nagayama spots (Uvulopalatoglossal spots )?
* How do you dx?
* What is the tx?

A

HHV 6 (6th Disease, Exanthema subitum)
* Replicates in leukocytes and salivary glands

Sxs: High Fever (104) for 3-5 days, febrile seizures, malaise, conjunctivitis, orbital edema, TM inflammation, LAD, irritability, anorexia, bulging fontanelle, diarrhea, cough, and URI symptoms
* Nagayama spots (Uvulopalatoglossal spots )- erythematous papules on soft palate and uvula.

Dx: Clinical and to r/o others

Tx: supportive, high risk of febrile seizures. Risk of recurrence in immunocompromised states (cancer/transplant etc.)

there is blenching in mouth

251
Q

What is the fever and rash presentation in roseola infantum?

A

After fever dissipates [day 5-6] rash develops [1-2days]
* 2-5mm rose-pink/red maculopapular appearance with halos, starting on trunk spreading to neck, face, and extremities.

252
Q

Parvovirus B19 (5th Disease)
* What is it not part of?
* The virus targets what? How is it transmitted?
* What is the incubation perood?
* What are the sx?

A
253
Q

5th Disease
* How do you dx? What can it cause?
* What is the txt?

A
  • Dx: Serology to detect Parvovirus B19 IgM (detectable within 7 days, may be positive for months)
    * Can cause “Glove and Sock” distribution of rash as well
  • Tx: Self-limiting

Be careful: sypillis, HFM, and 5th disease all cause glove and sock distribution

254
Q

What are the complications of 5th disease?

A

Aplastic crisis- inability to produce RBC leading to sudden and severe anemia
* In utero can cause fetal hydrops and CHF

255
Q

Influenza:
* What are the 3 types?
* How is it transmitted?
* What are the sxs?
* How do you dx?

A

Single stranded RNA virus (many subtypes, 2 most prevalent)
* A (Severe) – H1N1 Swine; H1N5 Avian;
* B (mild) – more seasonal
* C (rare) – not a typical test in clinical practice

Transmitted directly or indirectly via droplets or inanimate objects

Sxs: Typical respiratory (High fever, chills, headache, coryza, myalgia, flushed, hyperemic oropharynx, decreased appetite)
* Severe symptoms in immunocompromised patients

Dx: Clinical suspicion, Antigen vs PCR test

256
Q

How do you dx influenza?

A
  • RIDTs (Rapid Influenza Diagnostic tests) – nasal swab antigen detection w/i 3 days of onset, specific not sensitive, 15-30min results; good for outpatient use [false -], costly
  • Rapid molecular assay/ RT-PCR – detects viral RNA, can be used as a rapid for hospitalized patients or confirmatory with symptomatic false – RIDTs, detect nucleic acid with high sens/spec, 45 min – 2hr
  • EIA (Enzyme immunoassay) – detects A and B but not subtypes, 2 hours
  • Serology – not recommended, takes two + weeks
  • Viral culture – 4-10 days, used for characterization and identification for surveillance
257
Q

What is the tx of influenza?

A

Self-limiting in stable patient. Consider Tx in pregnant, elderly, abnormal vital signs, presence of abnormality on work-up (i.e. pneumonia). 72hr treatment window
* Antiviral medications for A and B: Oseltamivir (can be used as a prophylactic measure in high-risk areas or individuals), zanamivir, and peramivir
* Flu A: Amantadine, Rimantidine
* Flu vaccine yearly, educate on hand washing, hydration, symptom control

258
Q

Parainfluenza
* Multiple strains that causes what?
* What population is most common to get this?

A

Multiple strains, cause various upper vs lower respiratory symptoms
* Common cold, Croup, Tracheobronchitis, Bronchiolitis, Pneumonia
* Triggers Asthma, COPD, CHF

Community acquired for children < 5years old, immunocompromised, elderly, with predisposing factors:
* Malnutrition, overcrowding, Vitamin A def, environmental smoke or toxin

259
Q

What are the sxs of parainfluenza

A
260
Q

Parainfluenza:
* How do you dx?
* What is the txt?

A

Dx: Clinically, high level of suspicion during times of outbreak
* Molecular/PCR testing – most accurate
* Flocked swabs of nasopharynx during early illness and later on nasal aspiration/washes, sputum, lavage
* Viral Culture – rarely used, time consuming
* EIA – no rapid available

Tx: Depending on associated illness, supportive measures
* Croup – corticosteroids (PO/IM), nebulized epinephrine
* Humidifier, Hand hygiene, fluids
* Abx (only if have bacterial infection or pneumonia present)

260
Q

Measles (Rubeola):
* What is the incubation period?
* What is the pathophysiology? When can the disease be transimitted?
* What is the typical host?

A
  • Incubation 7-18 days
  • Penetrates into host cells (pharynx/lung), where the virus and cell create a matrix, thus regulating/suppressing host cell immune response, thus increasing viremia
  • Can be transmitted 4 days before and after 4 rash presence
  • Typical host – child 4-5yo (esp. those with Vit. A deficiency or malnutrition); pregnant or immunosuppressed.
260
Q

What is the difference of rubeola, rubella, roseola infantum?

A
260
Q

Measles (rubeola)
* What are the sxs? (prodromal, eruptive and convalescent stage)?

A

Sxs: 3 C’s = Cough, coryza, conjunctivitis; depletes vitamin A (epithelial cell damage); 4 D’s = rash starts on day 4
* Prodromal stage - fever, malaise, coryza, cough, conjunctivitis/photophobia, palpebral edema, dry cough; Koplik spots (white spots on buccal mucosa)
* Eruptive stage – high fever spikes with onset of maculopapular rash (fine ->coarse becoming confluent) which starts behind the auricle/hair line towards the face, trunk and extremities; fever disappears 2-3 days after rash starts
* Convalescent stage – 3-4 days after rash disappears, all symptoms dissipate in the way they appeared
* Atypical – high fever, HA, abdo pain, myalgia; pneumonia, otitis media, myocarditis, pericarditis, encephalitis

RASH IS LATER

261
Q

Measles (Rubeola)
* How do you dx?

A

Clinically
* Serology IgM (day 3 of rash - ~60days) and IgG (4 fold increase in Ab from acute to convalescent stage)
* RT-PCR – pharyngeal or nasopharyngeal swabs, urine; allows for genotyping
* Viral isolation

262
Q

How do you treat measles (rubeola)

A
  • Vitamin A (100-200k iu)
  • Symptom control, hydration, nutritional support, prevention of secondary infections
  • Routine Immunization (1st dose 12-15 mo, 2nd dose 4-6 y/o or 1 month after first dose if >12 mo)
263
Q

Measles

In patients without evidence of immunity and are exposed to measles, the following is recommended based on the patient’s clinical circumstances
* For infants 0 to 5 months of age:
* For infants 6 to 11 months of age:
* For children greater than 12 months of age:

A
  • For infants 0 to 5 months of age, it is recommended that they receive immune globulin within 6 days of exposure.
  • For infants 6 to 11 months of age, it is recommended that they receive either ameasles vaccination within 72 hours of exposure or immune globulin within 6 days of exposure.
  • For children greater than 12 months of age, who are unvaccinated, it is recommended that they receivemeasles vaccination within 72 hours of exposure (preferred over immune globulin). If the exposure occurred more than 72 hours, but within 6 days, the patient should receive immune globulin if they have not received at least one dose of themeasles vaccine (unless the child is severely immunocompromised, see below).
264
Q

Measles

In patients without evidence of immunity and are exposed to measles, the following is recommended based on the patient’s clinical circumstances
* Pregnant women without evidence of immunity:
* For immunocompromised patients:

A

Pregnancy
* It is recommended that they receive immune globulin.
* Measles vaccination, in conjunction with mumps andrubella, is contraindicated.

For immunocompromised patients:
* Immune globulin should be administered regardless of immunologic or vaccination status.

265
Q

Measles

In patients without evidence of immunity and are exposed to measles, the following is recommended based on the patient’s clinical circumstances
* Healthcare workers?

A
  • Two doses ofmeasles vaccine at the routine intervals should be administered for unvaccinated healthcare personnel regardless of the birth year who lack laboratory evidence of measles immunity or laboratory confirmation of disease.
  • Health care workers that lack evidence of immunity who were exposed to a patient withmeasles should be excluded from the workplace from day 5 through day 21 after exposure.
266
Q

German Measles (Rubella):
* How does it replicate?
* What are the sx?

A

Incubation period of 17-23 days; low grade fever, malaise, HA, sore throat, LAD, rash
* Rash begins, after fever, on face as pinpoint pink macules and papules (scarlatiniform or purpuric) and rapidly spread to trunk and extremities. [3 days]
* Forchheimer spots –petechiae on soft palate

RASH AFTER FEVER

267
Q

How do you dx rubella? (within 4 days of rash and in utero)

A
  • Serologic testing, EIA for IgM seen w/i 4 days of rash. IgG maybe used during acute exposure and convalescent phase
  • In utero: IgM in fetal blood or detection of rubella RNA via RT-PCR in amniotic fluid, fetal blood, chorionic villus bx
268
Q

How do you txt rubella?

A

Symptom control with use of NSAIDS
* In utero < 18 weeks – discuss pregnancy termination; >18 weeks – serial monitoring, US
* Children born with CRS need multidisciplinary approach
* Prevention through Vaccination

269
Q

How do yuo tell the difference btw rubella, measles, roseola (focus on fever and rash)

A
270
Q

Mumps:
* What is it caused by?
* What is the incubation period?
* What does it infect?

A
  • Caused by Rubulavirus via respiratory droplets
  • Incubates 7-21 days; Highly contagious 1-2 days before symptoms, then highly contagious
  • Infects mononuclear cells ->systemic inflammation in salivary glands, testes, ovaries, pancreas, mammary glands, CNS
271
Q

What are the different symptoms of mumps?

A
  • Prodrome – HA, fatigue, fever, anorexia, malaise
  • Followed by parotitis, orchitis; mild flat red rash; meningitis, encephalitis, myelitis, Guillan-Bare syndrome, cerebellar ataxia, facial palsy, hydrocephalus
  • Parotitis – MC manifestation 70%; Bilateral, painful inflammation between the earlobe and angle of the mandible
  • Stenson’s duct red, swollen, and involves the submaxillary and submandibular glands; Recurrent sialadenitis
  • Orchitis – bilateral painful swelling, enlargement, and tenderness of the testes -> testicular atrophy. Sterility is rare
272
Q

How do you dx mumps?

A

Dx: Clinically, plus labs
* RT-PCR serum or oral secretions, and for viral cultures
* Oral swab must be within 3-8 days of parotitis
* Serology for IgM and IgG – timing is everything. Vaccinated pt may result in false -; reportable CDC

273
Q

What is the txt and prevention of mumps?

A

Self resolving, Symptom control
* Cold compresses, pain management.
* Prevention through vaccination; live vaccine not for pregnant women,
* 5 day isolation

274
Q

Zika Virus:
* what virus? How is it transmitted?
* What are the areas that are predominate?
* What are the clinical presentations?
* What is congenital zika?

A
  • Arthropod-borne flavivirus
  • Transmitted by mosquito, sex, transfusion, maternal/fetal
  • Central, South America, Caribbean & Pacific
  • Clinical Presentation – most asymptomatic, about 20% have mild illness with low grade fever, rash, arthralgias, conjunctivitis.
  • Congenital Zika is devastating – microcephaly, cerebral malformation, ocular lesions, congenital contractures and hypertonia
275
Q
  • How do you dx zika virus?
  • What do you treat zika with?
A

Dx:
* Serum or urine Zika virus IgM, screen pregnant women with reverse-transcriptase PCR, NAAT

Txt:
* Supportive care, hydration
* Prevention –Avoiding mosquito bites, avoiding unprotected sex with a partner at risk of having Zika virus infection, and, for pregnant women, avoiding travel to areas with ongoing transmission.

276
Q

Ebola virus:
* What does it cause, how does it spread?
* What are the sxs?
* What does the ebola virus attack?
* What is the txt?

A
277
Q

Dengue Hemorrhagic Fever
* What is it due to?
* Endemic over where?
* What are the sxs?
* What are the labs?
* How do you dx?
* What is the tx?

A
278
Q

Norwalk Virus (aka Norovirus):
* Most common cause of what?
* How is it transmitted?
* What are the sxs?
* How do you dx?
* How do you treat this?

A
279
Q

What is TORCH? (think pregnancy)

A
280
Q
  • What is congential tozoplasmosis caused by?
  • What are the manifestations?
A
  • Congenital toxoplasmosis is caused by transplacental acquisition ofToxoplasma gondii
  • Manifestations (if present): Prematurity, intrauterine growth restriction, jaundice, hepatosplenomegaly, myocarditis, pneumonitis, rash, chorioretinitis, hydrocephalus, intracranial calcifications, microcephaly, and seizures
281
Q

Congenital toxoplasmosis:
* How is it diagnosised?
* What is the treatment?

A
  • Diagnosis is by serologic or PCR testing.
    * Forfetal infection,PCR analysis of amniotic fluid is emerging as the diagnostic method of choice
    * Serial IgG measurement (maternal infection)
  • Treatment is withpyrimethamine,sulfadiazine, and leucovorin.->PLS do not have tox while preg
282
Q

Syphilis in Pregnancy:
* What is the risk of transplacental infection?
* Likehood increases when?
* Which stages are transmitted more?
* Untreated syphilis in pregnancy is also associated with what?

A
  • Overall risk of transplacental infection of the fetus is about 60 to 80%
  • Likelihood is increased during the 2nd half of the pregnancy
  • Untreated primary or secondary syphilis in the mother usually is transmitted, but latent or tertiary syphilis is transmitted in only about 20% of cases
  • Untreated syphilis in pregnancy is also associated with a significant risk of stillbirth and neonatal death.
283
Q

Congenital syphillis:
* What is it?
* What are early signs?
* What are late signs?
* How do you diagnosis it?
* What is the treatment?

A
284
Q

Parvovirus B19 (5th Disease):
* What do children develop?
* Risk of what?
* Rarely, a baby will develop what?
* Testing is done mainly in who?
* What is the treatment?

A
285
Q

5th Disease During Pregnancy
* how do you monitor pregnant women with the infection?
* Aviod what?

A
  • There is no single recommended way to monitor pregnant women with parvovirus B19 infection.
  • Can get blood test to screen for disease or immunity
  • Avoid exposures inendemic areas or during outbreaks (workplace)
286
Q

Prenatal HSV-1
* When can genital herpes be transmitted?
* Risk is high enough that cesarean delivery is preferred in the following situations: (3)
* If women have recurrent herpes infections during pregnancy but no other risk factors for transmission, when can labor occur?
* What needs to be done when delivery is vaginal?
* What drug is safe during pregnancy?

A
287
Q

VZV: Pregnant Patient
* Approximately 10-20%of those infected with varicella developwhat?
* A pregnant mother can transmit varicella to her baby via what?
* If varicella develops during the first 12 weeks of pregnancy, the baby has a0.5-1% risk of developing what?
* If the virus is contracted between weeks 13 and 20, the baby has a 2%risk of having what?
* A baby with congenital varicella syndrome might have what?
* Varicella can develop when after delivery?
* If exposed and not immune, what should be done

A
288
Q

Varicella-zosterimmunoglobulin
* Varicella-zoster immunoglobulinis recommended for what?
* What are the different groups that might need it?

A
289
Q

What is the txt for varicella zoster (Congenital)

A
  • Primary – anti-viral – Acyclovir most common
  • Secondary Prophylaxis for recurrent infections – anti-viral initiated by patient at time of first sign/symptom
  • Secondary pharmaceutical therapies based on primary manifestation – Bells Palsy - Prednisolone
290
Q

Prevention of HSV?

A
  • Condom barrier protection during intercourse
  • Isolation, hand washing, gloves and gowns for care providers of patients with open lesions
  • Counseling patients to notify all partners and potential partners of status
291
Q

Congenital Rubella Syndrome (CRS)
* CRS in pregnancy can lead to what?
* What is super important for women to do before pregnancy and why?

A
  • CRS in pregnancy can lead to miscarriage or stillbirth, and increase risk of severe birth defects.
  • Although specific symptoms can be treated, there is no cure for CRS. Since there is no cure, it is important for women to get vaccinated before they get pregnant
292
Q

What are the most common birth defects from CRS?

A
293
Q

Rubella Vaccine Recommendations-CDC
* What vaccine should preg women not get?
* How long should preg women wait to avoid preg after getting MMR vaccine?

A
  • Because MMR vaccine is an attenuated (weakened) live virus vaccine, pregnant women who are not vaccinated should wait to get MMR vaccine until after they have given birth
  • Adult women of childbearing age should avoid getting pregnant for at least four weeks after receiving MMR vaccine.
  • Pregnant women should NOT get MMR vaccine, or rotavirus, chickenpox,small pox or yellow fever
294
Q

Congenital CMV Infection
* What are the signs at birth?
* If acquired later in infancy, signs may include what?
* How do you diagnosis?

A
  • Cytomegalovirus infection may be acquired prenatally or perinatally
  • Most common congenital viral infection
  • Signs at birth (if present: Intrauterine growth restriction, prematurity, microcephaly, jaundice, petechiae, hepatosplenomegaly, periventricular calcifications, chorioretinitis, pneumonitis, hepatitis, and sensorineural hearing loss
  • If acquired later in infancy, signs may include pneumonia, hepatosplenomegaly, hepatitis, thrombocytopenia, sepsis-like syndrome, and atypical lymphocytosis.
  • Diagnosis of neonatal infection is best made by viral detection via culture or PCR testing
295
Q

Congenital CMV Infection

What is the txt?

A

Mainly supportive
* Parenteral gancicloviror oral valganciclovirmay prevent hearing deterioration and improve developmental outcomes and is given to infants with symptomatic disease identified in the neonatal period

296
Q

CMV Prevention
* Nonimmune pregnant women should attempt to do what?
* Transfusion-associated perinatal CMV disease can be avoided how?

A
  • Nonimmune pregnant women should attempt to limit exposure to the virus. For instance, because CMV infection is common among children attending day care centers, pregnant women should always wash their hands thoroughly after exposure to urine and oral or respiratory secretions from children.
  • Transfusion-associated perinatal CMV disease can be avoided by giving preterm neonates blood products from CMV-seronegative donors or leukoreduced products.
297
Q

Congenital HPV
* A patient can get what?
* What can be found on cervical cancer screening?
* What can a mother do?

A
  • A patient can get genital warts or develop abnormal cell changes on cervix during pregnancy
  • Abnormal cell changes can be found with routine cervical cancer screening, which should continue during pregnancy
  • And a mother can transmit HPV to her baby during birth, but this is also uncommon-> for a female newborn, it will increase the risk of cervical cancer (16/18/35)
298
Q

Candidiasis
* What is it?
* can be cultured from what?
* What are the risk factors?
* WHAT IS A MAJOR FEATURE?

A
  • Normal flora becomes an opportunistic pathogen
  • Can be cultured from the mouth, vagina, and feces of most people
  • Risk factors – neutropenia, recent abd sx, broad spectrum abx, renal disease, IV catheters, cellular immunodeficiency
  • Scraping usually causes bleeding
299
Q

Esophageal canadsis
* What is the most frequent type?
* What is the clinical presentation?
* How is it diagnosis?
* What is the txt?

A
  • Esophageal involvement is the most frequent type of significant mucosal disease
  • Clinical presentation – painful swallowing (substernal), gastroesophageal reflux, nausea without substernal pain.
  • Diagnosis – endoscopy with biopsy and culture
    * KOH prep will reveal budding yeast
  • Treatment – fluconazole daily for 10-14d
300
Q
A
301
Q

Vulvovaginal candidiasis
* What is the clinical presentation?
* How it is diangosised?
* What is the txt?

A
  • Vulvovaginal candidiasis occurs in an ~75% of women.
  • Clinical presentation – acute vulvar pruritus, burning vaginal discharge, and painful sexual intercourse
  • Diagnosis –** Wet prep with KOH** visualize budding filaments and mycelia
  • Treatment – topical azole preparations –miconazole 200mg vaginal suppository for 3 days, or Fluconazole
302
Q

Invasive Candidiasis
* What has been approved for prophylazix of candida in neutropenic patients?

A
  • Bloodstream
  • Candidemia with deep-seated infection
  • Deep seated candidiasis in absence of bloodstream infection
  • Clinical presentation – varies from minimal fever to septic shock and can mimic a severe bacterial infection
  • Expect in immunocompromised patients
  • Requires ID consult
  • Note: Posaconazole has been approved for prophylaxis of Candida in neutropenic patients
303
Q

What is the test of choice for invasive candidasis?

A

Beta D-Glucan is the test of choice – indicates invasive fungal infection

304
Q

Cryptococcosis:
* Who is at the highest risk?
* Most common cause of waht?
* What is it caused by? Where is it found?
* What is the pathogenesis?
* What commons most often in setting of cellular immunodeficiency?

A
305
Q

Cryptococcosis-Clinical presentation
* Cryptococcosis usually presents clinically as what? What is the mechanisms?
* What happens with pulomary?
* What happens disseminated?
* What happens with CNS?
* What is present in 50%
* What are the DDX?

A
306
Q

Cryptococcosis:
* How do you dx respiratory disease?
* How do you dx meningeal disease?
* What does gram stain of CSF show?

A
307
Q

Clinical suspicion of crytococcosis when?

A

History of headache and neurologic symptoms in a patient with an underlying immunosuppressive disorder (HIV, organ transplant)

308
Q

Approach to Patient and Treatment:
* pulmonary cryptococcosis (pneumonia), with no evidence of extrapulmonary dissemination
* extrapulmonary (systemic) cryptococcosis, with or without meningoencephalitis

A
309
Q

What is the prevention of cryptococcosis?

A
310
Q

Blastomycosis
* What causes this infection?
* Seen primairy where?
* What are the sxs?
* How do you dx?
* what is the txt?

A
311
Q

Histoplasmosis:
* What causes it?
* How is it transmitted?
* What are common areas?
* What is the aptho?
* What spreads to other organs?

A
312
Q

Histoplasmosis:
* Most people are what?
* Past infections leaves what?
* What are mild sxs?
* What are mod severe diseases present as?

A
  • Most are asymptomatic, go unrecognized
  • Past infection leaves pulmonary and splenic calcification
  • May involve soft tissues
  • May have a mild flu-like-illness
  • Moderately severe infections have a clinical picture of pneumonia with fever, cough and mild central chest pain lasting 5-15 days
313
Q

Diagnostics of Histoplasmosis
* What is shown on CBC?
* What is increased?
* What test is there
* What can be cultured?
* What does the cxr show?

A
  • Pancytopenia on CBC
  • Increased alkaline phosphatase and LDH
  • Antigen test – sputum or urine
  • Blood or Sputum Cultures
  • CXR – pulmonary infiltrates, hilar or mediastinal lymphadenopathy
314
Q
  • What is the txt of histoplasmosis?
  • AIDS related histo requires what?
A
  • In most cases Itraconazole OR AmB + Itraconazole (for severe disease)
  • AIDS related histoplasmosis requires life long suppressive therapy.
315
Q

Pneumocystis jirovecii
* Acute interstitial plasma cell pneumonia that occurs among two groups ?
* Occurs in up to 80% of what population?
* What is the pathogenesis?
* What is the lung pathology?

A
316
Q

How did P. jiroveciipneumonia have an interesting start?

A
317
Q

What is the clinical presentation of P.jirovecii?

A
  • Fever with non-productive cough
  • Progressive dyspnea on exertion
  • Physical signs may be minor; nonspecific
  • Bibasilar crackles (may develop later)
  • Extrapulmonary manifestations: Rare, most notably include lymph nodes, hepatosplenomegaly
318
Q

dx of P. jirovecii
* CXR shows what?
* What does CT show?
* What does ABG show?
* Cultured?
* PCR?
* What do the labs show?
* What does the gram stain show?

A
319
Q

What does this show?

A
320
Q

Treatment of PCP:
* If the disease is suspected clinically, appropriate to start what?

A

to start empiric therapy
* Oral trimethoprim-sulfamethoxazole x 14 days is the preferred agent for mild-moderate disease

321
Q
A
322
Q

Coccidiomycoses:
* What does it cause?
* What does it cause in patient with CD4 less than 250?
* What is the txt?

A
323
Q

Aspergillosis:
* Typically will cause what? May cause what?
* What is a high risk population?
* What are the sxs?
* How do you dx?
* What is the tx?

A
324
Q

What are the 2 phylas of helminthics?

A
325
Q
A
326
Q

Helminth Infestations
* What is themc helminth infection globally?
* What is the transmission?
* What is the clinical presentation early?
* How do you dx?
* What is the tx?

A
327
Q

Cestodes (tapeworms):
* Infected by what? Where does it develop and attaches to?
* Adult tapeworms are what?
* Tapeworms do not have what?
* Pieces of tapeworm expelled via what?
* What are the sxs?
* What is the txt?

A
328
Q

Trematodes:
* What are the different types?
* Adult flukes are often what?
* Flukes are hermaphroditic except for what?
* Eggs are passed how?
* How is it transmitted to humans?
* What are the clinical sx and tx?

A
329
Q

Pinworms:
* What is the species?
* What is the cardinal sign?
* How do you dx?

A
  • Enterobius vermicularis
  • Cardinal sign – perianal pruritis, typically nocturnal
  • Diagnosis – identification of eggs or adult worms on perianal skin
    * Scotch tape test
330
Q

What is the txt of pinworms?

A
  • Treatment – Albendazole 400mg or Pyrantel pamoate 11mg/kg to max of 1 gram (caution <2yo), mebendazole 100mg – all single doses
  • Repeat dose in two weeks due to frequent reinfection
  • Wash all cloths and bedding
  • Treatment of household members is advocated to eliminate asymptomatic reservoirs of potential reinfection
331
Q

Hookworms:
* Eggs passed how?
* Larvae penetrate what?
* Larvase mature/live where?
* How do you dx?
* What is the tx?

A
332
Q

Malaria:
* Most important what?
* Endemic where?
* 4 species of the genuses of what?
* What genus is responsible for nearly all severe disease?
* How is it transmitted?

A
333
Q

Pathogenesis of malaria
* Mosquitoes inject what? Where does this go and do?
* What is released from the liver and what do they do?

A
334
Q

Transmission & Risk of malaria:
* Uncommonly transmitted from what?
* _ transfusion
* Relapses likely due to what?
* What people are high risk for severe disease?

A
335
Q

Clinical findings of malaria:
* Prodrome of what?
* Classic findings?
* What are other sx?
* What happens from fever or CNS disease?
* What does the exam show?
* What is the not typical in malaria?

A
336
Q

Malaria:
* how must be evaluated for malaria?
* Sereve disease has waht?
* It might take how long to see sx?
* Malaria is the most common cause of what?

A
337
Q

Lab Findings of malaria:
* What is the mainstay of diagnosis?
* When should a repeat smear happen?
* What is widely available but not well standardized?
* What mean indicate history of disease but are not useful for diagnosis?
* PCR?
* Severe malaria may cause what?
* What does the CBC show?

A
338
Q

Treatment of malaria:
* What is the standard of care?
* What is the old standard?
* What is available via CDC in US?
* What is the dosing of Artesunate
* What do you give for uncomplicated malaria?

A
339
Q

Toxoplasmosis
* What is the cause?
* How are the hosts?
* Humans are infected by what?

A
  • Cause – T. gondii
  • Hosts – cats
  • Humans infected by ingestion, food or water contaminated by cats, transplacental, transfusion or organ transplant
  • ~1.1 million in US, vision loss in 4800
340
Q
A
341
Q

Clinical Findings & Treatment of Toxoplamosis:
* Most people are what?
* When do people become sxs?
* What may last for months?
* What are the sxs?
* What are severe sxs?

A
342
Q

Congenital Tox Infection:
* Early fetal infections commonly result in what?
* Most infants will appear how at birth?
* The most common late presentation of congenital toxoplasmosis is what?

A
343
Q

Diagnosis, Treatment, Prevention of tox
* Confirmed by what?
* Multiple serologic methods like what?
* Medications do not do what? and immunocompetent persons infected do not need what?
* If severe sxs, what is the txt?

A
  • Confirmed by isolation of Toxoplasma gondii or identification of tachyzoites in tissue or body fluids
  • Multiple serologic methods – IgM and IgG most sensitive
  • Medications do not eradicate disease and immunocompetent persons infected do not typically require tx
  • If severe sxs: Generally treat for 1 month with pyrimethamineplus either sulfadiazine or clindamycinand sometimes with prednisone
344
Q

Tox:
* What is the txt in pregnancy?
* What is the preventation?

A
  • Treatment required in Pregnancy
    * Pyrimethamine and sulfadiazine, plus folinic acid (Leucovorin)
    * Alternatives are available, but are inferior to pyr-sulf
  • Prevention – avoid cats, avoid undercooked meat, pregnant women should not empty litter boxes
345
Q

Amebiasis (DYSENTERY):
* What is it due to? Who should you consider?
* What are the sx? What will you see on CT?

A
  • Due to fecal/oral transmission of Entamoeba histolytica
    * Consider in recent travelers or immigrants
  • See diarrhea, abdominal pain, weight loss, hepatomegaly/RUQ pain.
    * On CT will see oval lesions in the liver – if aspirate see “anchovy paste” appearance.
346
Q

Amebiasis (DYSENTERY)
* How do you dx?
* What is the tx?
* What do you order for asymptomatic liver cysts order

A
  • Dx by Stool O&P, antigen tests or FNA if cysts on skin.
  • Tx Metronidazole or tinidazole and Paromomycin.
    * If asymptomatic liver cysts order PO ABX – iodoquinol or paromomycin
347
Q
A

Clinical Medicine 1 (8 decks)

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