MS Infectious Disease Flashcards Preview

Skin MS: Week 6 > MS Infectious Disease > Flashcards

Flashcards in MS Infectious Disease Deck (160):
1

 infection leading to the necrosis of subcutaneous tissue.  Severe pain is common.  Infection should be treated very seriously and aggressively through surgery and IV antibiotics and fluids.

Nectrotizing Fasciitis

2

Most common causative agent of necrotizing fasciitis

Strep pyogenes

3

rapidly progressing joint infection.  Usually bacterial in origin.

Acute infectious arthritis

4

Most common causative agent acute infectious arthritis

Staph aureus

(N. gonorrhea in sexually active young people)

5

inflammation and destruction of bone caused by bacteria, mycobacteria, or fungi.  Causes localized bone pain and tenderness.  80% of infections result from contiguous spread or from open wounds.

Osteomyolitis

6

infection of the muscle that leads to muscle inflammation.  Can be caused by many different microorganisms including viruses, bacteria, and helminthes.

Myositis

7

Presence of bacteria in bloodstream

bacteremia

8

Viremia

presence of virus in bloodstream

9

bloodborne systemic infection.  Can lead to spread of the infectious organism to other tissues, massive inflammation, septic shock, and rapid death.  Associated with bacterial infections

Septicemia

10

3 ways for bacteria to initiate infection

1.Breach the skin

2.Systemic disease

3.Toxin-mediated damage

11

Life-threatening infection of subcutaneous tissues, most often caused by beta-hemolytic, group A Streptococcus (Streptococcus pyogenes) and to a lesser degree Staphylococcus aureus and other microorganisms.

Necrotizing fasciitis

12

"Flesh-eating bacteria", toxin mediated disease

Necrotizing fasciitis

13

Necrotizing Fasciitis: Life-threatening infection of ________ tissues, most often caused by ____-hemolytic, _________ and to a lesser degree __________ and other microorganisms. Can be ____________.

•Life-threatening infection of subcutaneous tissues, most often caused by beta-hemolytic, group A Streptococcus (Streptococcus pyogenes) and to a lesser degree Staphylococcus aureus and other microorganisms. Can be polymicrobial. 

14

Nectrotizing fasciitis: More than 50% of patients have experienced a recent _____, _______, or _______ infection.

More than 50% of patients have experienced a recent minor trauma, surgery, or varicella infection.

15

Nectrotizing Fasciitis: Can result in widespread _______ of the skin, ______, ________, and _____.

Can result in widespread desquamation of the skin, shock, multiorgan failure, and death.

16

NF: The infection tends to begin with a _____, _____, or _______ that extends from superficial skin layers down through fascia and muscle.

The infection tends to begin with a break in the skin, invasion, or deep blunt trauma (hematoma) that extends from superficial skin layers down through fascia and muscle.

17

NF: Tx

Aggressive surgical intervention is required to prevent the spread of infection, in addition to antibiotics.

18

Gas gangrene vs NF

GG has crepitance (gas formation) 

19

Streptococcus Pyogenes tree

Bacteria - Gram+ - Cocci - Catalase (-) - beta-hemolytic - bacitracin sensitive 

20

Bacteria - Gram+ - Cocci - Catalase (-) - beta-hemolytic - bacitracin sensitive 

Streptococcus pyogenes (NF)

21

Strep Pyogenes virulence factors

streptokinase, M protein, hyaluronidase, Dnase.

22

Necrotizing Fasciitis sxs 

High fever

High heart rate

Altered mental status

Low blood pressure

Leukocytosis (high white blood cell count)

Positive blood cultures

23

Dx of NF

•Rapid onset

•High CRP

•High ESR

•High WBC with banded neutrophils

•CT imaging could reveal edema of the soft tissues

•Gram stain the wound

•Culture the wound (sample taken during surgery) and blood

•Surgical debridement of necrotic tissue

24

WBC measures ____

Leukocytes per mL blood

25

WBC high counts --> 

high counts during infections, inflammatory diseases, autoimmune systemic diseases, leukemia, and emotional and physical stress.

26

Normal Range WBC

4500-11000 cells/mL

27

Banded neutrophil

Committed to neutrophil pathway - but not fully mature. LEFT SHIFT. Sign of severe acute infection.  

28

Normal WBC differential 

 

Basophils ≤ 2%

Eosinophils ≤ 5%

Lymphocyte 22 – 44% (high in viral infections, tuberculosis, typhoid)

Monocytes 3 – 9%

Neutrophils 40 – 60% (high in acute bacterial infections, others.  Bands = immature neutrophils “left shift”)

29

Lymphocytes high in _

Viral infections, tuberculosis, typhoid

30

Neutrophils high in _

Acute bacterial, others. Banded -- severe.

31

ESR

Erythrocyte Sed Rate

Rate at which red blood cells precipitate in a period of 1 hour when anti-coagulated blood is allowed to stand.  Rough measure of abnormal acute phase proteins and immunoglobulins.  Nonspecific indicator of tissue damage and inflammation.

32

Normal ESR

<= 20mm/hr

33

ESR elevated in _

anemia, endocarditis, kidney disease, osteomyelitis, pregnancy, and many others.

34

C-Reactive Protein

Produced in the liver and is present in circulation at low levels normally.  Involved in the promotion of the immune system through the activation of the complement cascade.

 

35

Normal CRP

<= 1mg/dL

36

CRP elevated in _

bacterial infections, inflammation conditions, acute rheumatic fever, acute rheumatoid arthritis, inflammatory bowel disease, and others.

37

Synovial fluid changes in acute infectious arthritis

Change in color to more yellow

More cloudy/opaque 

May be hemorrhagic (d/t virulence factors of infectious agent) --> blood in synovial fluid (red)

38

Sxs Acute Infectious Arthritis

Rapid onset

Personal history

Pain

Range of motion restriction (single joint)

Synovial fluid analysis and culture

Positive blood cultures

39

Bacteria

Gram +

Cocci

Catalase +

Coagulase +

 

Bacteria

Gram +

Cocci

Catalase +

Coagulase +

Staphylococcus aureus

40

Staph aureus tree

Bacteria

Gram +

Cocci

Catalase +

Coagulase +

Staphylococcus aureus

41

Bacteria

Gram (-)

Diplococci

Oxidase (+)

Only Glucose Oxidizer

 

Bacteria

Gram (-)

Diplococci

Oxidase (+)

Only Glucose Oxidizer

Neisseria gonorrhoeae

42

Neisseria gonorrhoeae tree

Bacteria

Gram (-)

Diplococci

Oxidase (+)

Only Glucose Oxidizer

Neisseria gonorrhoeae

43

N. gonorrhoeae like to be in _____ cells

Neutrophils

44

Staph aureus virulence factors

protein A, coagulase, hemolysins, leukocidins, hyaluronidase, staphylokinase, lipase.

45

N. gonorrhoeae virulence factors

Specialized pili – allows attachment to mucosal surface, antigenic variation to evade host defenses, prevents phagocytosis.

Endotoxin.Capsule.IgA protease.

46

Osteomyelitis sxs

Acute - weight loss, fatigue, fever, localized warmth, erythema, tenderness. May form subcutaneous abcesses which drain spontaneously through skin. Chronic - intermittent bone pain, tenderness, draining sinuses.

47

tx osteomyelitis

Abx, surgery to remove abcesses, potential spinal instability or necrotic bone.

48

Osteomyelitis --> _________ in bone

Abcesses 

49

Osteomyelitis - differential 

Skin infections may be deep seated with an abscess, or mainly cellulitis (superficial redness and warmth).

Gas gangrene would have crepitance on palpation due to the presence of gas.

Skin cancers may manifest with similar lesions, but usually in older individuals.

Sarcomas may manifest with skin or soft-tissue lesions.

TB classically causes osteomyelitis of the vertebrae, called Pott disease, although other areas may be seen; overlying cellulitis is uncommon in such cases.

S. aureus is the most common cause of skin and soft-tissue infections.

50

TB causes __________ (often as losing control of ds)

Osteomyelitis (also encephalitis) - but usually vertebrae (Pott disease)

51

Most common cause of skin/soft-tissue infection --> osteomyelitis

Staph aureus

52

Bacteria

Gram -

Coccobacilli (pleomorphic)

Oxidase +

Catalase +

Pasteurella multocida

53

Where get Pasteurella multocida?

Cat bite (normalized flora)

54

Bacteria

Gram -

Bacilli

Lactose non-fermenter

Oxidase –

Produces H2S

Motile

Salmonella typhii

55

Salmonella typhii tree

Bacteria

Gram -

Bacilli

Lactose non-fermenter

Oxidase –

Produces H2S

Motile

56

Salmonella typhii and osteomyelitis predisposing factor

Sickle cell anemia - Salmonella super invasive but normal blood cell people could typically clear quickly, but sickle cell --> lack of complement 

Alternative --> C3 catalyzes own breakdown on cell surface into C3b which goes into bloodstream – start to bind stuff – target S. typhii

Sickle Cell – complement receptor localizes in pocket of RBC before pathogen bound (trapped)

 

57

Pasteurella multocida tree

Bacteria

Gram -

Coccobacilli (pleomorphic)

Oxidase +

Catalase +

58

Salmonella, Sicke Cell and osteomyelitis

combination of expanded marrow in sickle cell patients together with high oxygen demand and sluggish circulation means that bone is vulnerable to infarction.

Infarcted areas act as loci for infection.

Gut devitalization due to intravascular sickling leads to an increased incidence of invasion and bacteremia.

Sickle cell patients have reduced bactericidal and opsonic activity against Salmonella and an abnormality in the alternative pathway of complement activation.

59

Bacteria

Gram +

Bacilli

Spore-forming

Obligate anaerobe

Non-motile

Clostridium perfringens

60

C. perfringens tree

Bacteria

Gram +

Bacilli

Spore-forming

Obligate anaerobe

Non-motile

61

Myositis causative agents

C. perfringens, Staph aureus, coxsackievirus A and B, Dengue Fever virus, Taenia solium, Trichinella spiralis

62

Virus

ssRNA (+), Group IV

Nonsegmented

Icosahedral Nucleocapsid

Nonenveloped

Picornaviridae

Enterovirus

Coxsackievirus A and B

63

Coxsackievirus A and B tree

Virus

ssRNA (+), Group IV

Nonsegmented

Icosahedral Nucleocapsid

Nonenveloped

Picornaviridae

Enterovirus

64

Virus

ssRNA (+), Group IV

Nonsegmented

Icosahedral Nucleocapsid

Enveloped

Flaviviridae

Dengue Fever Virus (Flavivirus)

65

Dengue Fever Virus tree

Virus

ssRNA (+), Group IV

Nonsegmented

Icosahedral Nucleocapsid

Enveloped

Flaviviridae

66

Helminth

Transmitted by ingestion

Intestinal and tissue infection

Platyhelminthes (flatworms)

Cestodes (tapeworms)

 

Taenia solium 

67

Taenia solium tree

Helminth

Transmitted by ingestion

Intestinal and tissue infection

Platyhelminthes (flatworms)

Cestodes (tapeworms)

Taenia solium

68

Helminth

Transmitted by ingestion

Tissue infection

Nematodes (roundworms)

Trichonella spiralis

69

Trichinella spiralis tree

Helminth

Transmitted by ingestion

Tissue infection

Nematodes (roundworms)

70

This infection is typically caused by a mixture of aerobic and anaerobic organisms leading to the necrosis of subcutaneous tissue.  Signs of infection include tissues that become hot, red, and swollen, resembling severe cellulitis.  Severe pain is common.  Without timely treatment the area of infection becomes gangrenous.  Patients present acutely ill.  Diagnosis is through history and examination, supported by evidence of overwhelming infection.  Treatment includes antibiotics and surgical debridement.  Prognosis is poor without early aggressive treatment.

Necrotizing Fasciitis

71

severe muscle pain is the hallmark of _____________ (myositis)

pleurodynia (coxsackievirus B), trichinellosis, and bacterial infection

72

Only non-motile Clostridium member

Clostridium perfringens

73

NF treatment

Abx and surgical debridement

74

Most NF cases result from infection with _____

group A streptococcus (Streptococcus pyogenes) or a mixture of aerobic and anaerobic bacteria (Bacteroides species)

75

NF: 

The primary symptom of infection is ____________.  Tissue is __, ___, and ____ and rapidly becomes ____.  

Bullae, crepitus (resulting from soft tissue gas), and gangrene may develop.  

_______ necrose but muscles are spared initially.  Patients present _______ with a high ____, high ____, altered ______, and low ______.  Patients may be ________.  ____________ may develop.

The primary symptom of infection is intense pain (pain out of proportion of clinical findings).  Tissue is hot, red, and swollen and rapidly becomes discolored.  Bullae, crepitus (resulting from soft tissue gas), and gangrene may develop.  Subcutaneous tissues necrose but muscles are spared initially.  Patients present acutely ill with a high fever, high heart rate, altered mental status (confusion), and low blood pressure.  Patients may be bacteremic or septic.  Streptococcal toxic shock syndrome may develop.

76

NF Dx 

History and examination and is supported by _____, _____ on x-ray, _____ blood cultures, and deteriorating ____ and ______ status.  

Diagnosis is made by history and examination and is supported by leukocytosis, soft-tissue gas on x-ray, positive blood cultures, and deteriorating metabolic and hemodynamic (blood pressure) status.  

77

NF affects what tissues

SubQ necrosis - but muscles are initially spared (may turn into myositis)

78

Common organisms causing Acute infectious arthritis classified as ____ or _____ in adults

gonococcal or nongonococcal

79

AIA: ______ infections are far less destructive to the joint

gonococcal infections are far less destructive to the joint

80

AIA: Adolescents and adults

Gonococci (young, sexually active adults), nongonococcal bacteria (Staphylococcus aureus, streptococci)

 

Cervical, urethral, rectal, or pharyngeal infection with bacteremic dissemination – gonococci.

Bacteremia – staphylococci and streptococci

81

AIA: Neonates

 

Group B streptococci, Escherichia coli, Staphylococcus aureus

Maternal-fetal transmission; IV punctures or catheters with bacteremic dissemination

82

AIA: Children =<3

 

Streptococcus pyogenes, Streptococcus pneumoniae, Staphylococcus aureus

Bacteremia (otitis media, URIs, skin infections, meningitis, etc)

83

AIA: 3-adolescence

 

Staphylococcus aureus, streptococci, Neisseria gonorrhoeae, Pseudomonas aeruginosa, Kingella kingae

Bacteremia or contiguous spread

84

AIA: All ages

 

Viruses (parvovirus B19, HBV, HCV, rubella virus, VZV, mumps virus, adenoviruses, coxsackieviruses A and B, HIV, EBV)

Viremia or immune complex deposition

85

AIA: Pt w/ possible tick exposure

 

Borrelia burgdorferi (Lyme disease)

Bacteremia

86

AIA: Pt w/ bite wound

 

Often polymicrobial.  

Human bites – Eikenella corrodens, group B streptococci, Staphylococcus aureus, oral anaerobic bacteria.  

Dog and cat bites – Staphylococcus aureus, Pasteurella multocida, Pseudomonas species, Moraxella species, Haemophilus species.

Rat bites – Staphylococcus aureus, Streptobacillus moniliformis, Spirillum minus

 

 

Direct joint penetration, usually of the small joints of the hands

87

AIA: The elderly, patients with severe joint trauma or serious disease (immunosuppression, hemodialysis, SLE, RA, diabetes, cancer)

 

Staphylococci (particularly in RA), gram-negative bacteria, Salmonella species (particularly in SLE)

Urinary tract, skin

88

GC arthritis sxs

fever (for 5 to 7 days), multiple skin lesions on the mucosal surfaces and on the trunk, hands, or lower extremities.  Inflammatory arthritis in one or more joints also occurs often in the hands, wrists, elbows, knees, and ankles.

89

Other AIA symptoms

progressive moderate to severe joint pain that is markedly worsened by movement.  Most infected joints are swollen, red, and warm.  Fever is absent or low in about 50% of patients.  In 80% of adults, nongonococcal bacterial arthritis is monoarticular.  In infectious arthritis due to bite wounds symptoms typically develop within 48 hours.  Rat bites tend to cause systemic symptoms including fever, rash, and joint pain within about 2 to 10 days.  Viral infectious arthritis causes symptoms that can be similar to nongonococcal arthritis and is more likely to be polyarticular.

90

AIA dx

arthrocentesis with synovial fluid examination and culture, blood culture, imaging studies, CBC and ESR (or CRP).  Synovial fluid examination is key.  Fluid is sent for cell count and differential, Gram stain, culture, and crystals.  Foul-smelling synovial fluid suggest anaerobic infections.  Fluid from an acutely infected joint will have a WBC of greater than 20,000/μL consisting of greater than 95% PMNs.  Gram stain results are suggestive of the causative microorganism but cultures are definitive.  The presence of crystals does not rule out infectious arthritis. ​

91

________ can destroy articular cartilage, permanently damaging the joint.

Acute nongonococcal arthritis can destroy articular cartilage, permanently damaging the joint.

92

_________ accounts for 50% of cases of viral myocarditis.

Coxsackie B virus accounts for 50% of cases of viral myocarditis.

93

Coxsackie B pathology: infections are typical in_______ (seasonal) and the virus is transmitted via ________ or ________. The virus travels in the ______ and infects ___________. Local replication ensues and virus spreads in the ________. From here the virus infects and can lyse ______ and _______ surfaces to cause ____________ (3).

infections are typical in summer and fall and the virus is transmitted via aerosols or fecal to oral route. The virus travels in the G.I. tract and infects mucosal epithelial cells. Local replication ensues and virus spreads in the bloodstream. From here the virus infects and can lyse heart and pleural surfaces to cause pleurodynia, myocarditis, and pericarditis.

94

Coxsackievirus: In Group A and B infections the virus can travel to the _______ and __________ to cause ________ and _______.

In Group A and B infections the virus can travel to the meninges and anterior horn motor neurons to cause meningitis and paralysis.

95

Cox B dx

isolate virus, serology.

96

Cox B tx

Symptomatic infections – anti-inflammatory agents.  No antivirals or vaccines available.

97

Dengue Fever Virus: geographic location

This virus is found in the tropics worldwide. Dengue hemorrhagic fever is most common in southern Asia.

98

DFV: Clinical Presentation

 

Dengue fever – “breakbone fever” (flu-like with severe joint and muscle pain).  

Dengue hemorrhagic fever – (dengue fever with hemorrhage and shock).

99

DFV

____, _____, and ______ are all normal reservoirs for this virus. It is transmitted through ________ and enters the ______ to cause __________. From here the virus infects _________ causing acute inflammation release of __________ and _________ to create “____________”. If this initial infection is followed by a second infection of a different serotype, then ________ from the first serotype infection _________ and ________ to form ___________ and a ___________ which can lead to ________ and _________ (_________).

humans, monkeys, and birds are all normal reservoirs for this virus. It is transmitted through a mosquito bite and enters the bloodstream to cause transient viremia. From here the virus infects macrophages causing acute inflammation release of pyrogens and pain mediators to create “breakbone fever”. If this initial infection is followed by a second infection of a different serotype, then antibodies from the first serotype infection increase and cross-react to form immune complexes and a type III hypersensitivity reaction which can lead to hemorrhage and shock (Dengue Hemorrhagic Fever).

100

How pathogens get into joints for AIA?

Infectious organisms reach the joints by direct penetration (trauma, bites, surgery, etc), extension from an adjacent infection (osteomyelitis, abscess, infected wound, etc), or hematogenesis spread from a remote site of infection.

101

______ are major host defense system in AIA but also the cause of joint damage

PMNs

Neutrophils, eosinophils, and basophils are polymorphonuclear leukocytes. A polymorphonuclear leukocyte is a type of white bloodcell. Also called granular leukocyte, granulocyte, and PMN.

102

Osteomyelitis dx

ESR, CRP, Xray, MRI, radioisotropic bone scanning, culture bone/abcess formation. Suspect if localized peripheral bone pain, fever, malaise or localized refractory vertebral pain. PE. Need to dx specific bacteria.

103

Osteomyelitis pathogenesis/location 

Bone - may occlude local blood vessels --> bone necrosis and local spread of infection. Bone cortex, under periosteum, formation of subcutaneous abcesses.

104

Myositis dx

temporal progression of lesions, travel hx, animal exposure/bite hx, age, underlying ds, lifestyle. Soft tissue radiography, CT, MRI.

105

Leading cause of osteomyelitis in children and adults

Staphylococcal aureus

106

Coxsackie A vs B/A

B - pleurodynia, myocarditis, pericarditis

A + B - aseptic meningitis, paralysis, URT infection

107

Tricuspid valve endocarditis

Frequent in IV drug users, staph aureus

108

Patients w/ granulomatous ds are vulnerable to ______

staph aureus

109

Staph aureus clinical presentation

Local: skin/subQ- impetigo, cellulitis, folliculitis, furuncles, carbuncles. 

Respiratory: pneumonia w/ cavitations

Systemic: acute endocarditis, meningitis, osteomyelitis, septic arthritis

110

Staph Aureus pathology: Bacteria colonize _____ or _____ (how) →  overgrow and evade host defenses using ____, _____, _____, and _____.  _____ localize to site of infection →  _______ form →  ________ infections or _____ results.  Deeper invasion into the bloodstream relies on the _____, ______, and _____ virulence factors.

Bacteria colonize skin (following breach) or nasopharynx (following intubation or viral infection) →  overgrow and evade host defenses using protein A, coagulase, hemolysins, and leukocidins.  Neutrophils localize to site of infection →  purulent abscesses form →  skin/subcutaneous infections or pneumonia results.  Deeper invasion into the bloodstream relies on the hyaluronidase, staphylokinase, and lipase virulence factors.

111

Staph aureus dx

Blood culture for Gram +, catalase +, coagulase + 

112

Staph aureus tx

Abx - penicillinase-resistant penicillins or vancomycin

113

Obligate human pathogens

Neisseria gonorrhoeae

Salmonella Typhi

114

N. gonorrhoeae high incidence w/ 

menstruation, IUDs, sexually active

115

N. gonorrhoeae: __________ prevents immunity allowing recurrent infections

Antigenic variation (d/t specialized pili)

116

N. gonorrhoeae clinical presentation 

Local infection = (genital tract or anorectal infections) either asymptomatic, urethritis, dysuria (men), cervicitis (women), opthalmia neonatorum.  

Systemic = septic arthritis.  

Complications = Pelvic Inflammatory Disease (PID), ectopic pregnancy, sterility, Fitz-Hugh-Curtis Syndrome

117

N. Gonorrhoeae pathology 

Colonization begins when bacterial ___ attach to mucosal cells of ____ and ____.  Evades mucosal _______ via _______.  _____ by _______ and kills _________ --> inflammatory response leading to _______ (men) and _____ (women).

In women, infection can progress to _____, ______, ________ which can lead to increased risk for _____________.  From _______  bacteria can spill into the __________ causing _______.  This can lead to an infection of the ________ (Fitz-Hugh-Curtis Syndrome).

Colonization begins when bacterial pili attach to mucosal cells of urethra and vagina.  Evades mucosal IgA antibodies via IgA protease.  Endocytosed by immune cells and kills ciliated cells --> inflammatory response leading to urethritis (men) and cervicitis (women).

In women, infection can progress to uterus, fallopian tubes, and ovaries (PID) which can lead to increased risk for ectopic pregnancies.  From fallopian tubes bacteria can spill into the peritoneal cavity causing peritonitis.  This can lead to an infection of the liver capsule (Fitz-Hugh-Curtis Syndrome).

118

N. gonorrhoeae: Septic Arthritis pathogenesis

The bacteria can also invade the _____ and enter into the ______ where it can collect in ________ causing septic arthritis.

The bacteria can also invade the submucosa and enter into the bloodstream where it can collect in synovial fluid causing septic arthritis.

119

N. Gonorrhoeae in neonates 

Can inoculate the conjunctiva during passage through the birth canal causing opthalmia neonatorum  --> risk for blindness.

120

N. gonorrhoeae DX 

Gram (-) diplococci within PMNs, metabolizes glucose but not maltose, selectively grows on Thayer-Martin media.

121

NG TX

Ceftriaxone (+ doxycycline for probable concurrent Chlamydia infections), prophylactic erythromycin eye drops for neonates.  Vaccine development difficult.

122

Salmonella Typhii virulence factors 

H antigen (flagella), endotoxin, Vi capsule.

123

Susceptible to Salmonella typhi

Sickle-cell patients are functionally asplenic and have trouble clearing Vi-encapsulated Salmonella.  

Patients with impaired gastric acid secretion are more susceptible.

124

Complication of S. typhi 

Because S. typhi are stored well in gallstones, carriers may present with S. typhi-induced necrotizing cholecystitis

125

Clinical presentation S. Typhi

 asymptomatic carrier state, typhoid fever (enteric fever), osteomyelitis in sickle cell patients.

126

S. Typhi Pathology: 

Spread through _______ transmission.  Large inoculum overcomes the ______.  Bacteria penetrates the ________ barrier in the ________ which leads to transient _____________.

______________ (VF) allows survival in _______ of ________.  Spread via ______ to the ______, _______ and _______  where ________  is then released.  This creates ______  on the _______ , _____ , ______, and ________ (typhoid fever).  This infection can then progress into the ________ or it may ___________.

Spread through fecal-to-oral transmission.  Large inoculum overcomes the gastric acid defense.  Bacteria penetrates the mucosal barrier in the distal ileum or colon which leads to transient asymptomatic bacteremia.

Capsular Vi polysaccharide allows survival in phagocytes of Peyer’s patches.  Spread via phagocytes to the gallbladder, liver, and spleen where endotoxin is then released.  This creates rose spots on the abdomen, fever, diarrhea, and abdominal pain (typhoid fever).  This infection can then progress into the carrier state or it may self-resolve.

127

S. typhi carrier state 

the bacteria are stored in the gallbladder, especially in gallstones.  The bacteria may reenter the bowel lumen to generate more microorganisms that can spread through contaminated feces.

128

S. typhi dx 

Gram (-) rod cultured from the blood.  Motile by flagella.  Produces hydrogen sulfide.  Does not ferment lactose.

129

S. typhi tx and caveat

Ceftriaxone for resistant strains.  Ciprofloxacin and ampicillin for carriers.  Cholecystectomy may be necessary for carriers.  Two oral vaccines are available for travelers (killed or live-attenuated).

Treating S. typhi infections may actually increase the risk for reinfection due to interference of the development of a suitable host immune response.

130

Pasteurella multocida clinical presentation

cellulitis, osteomyelitis following cat and dog bites.

131

Pasteurella multocida pathology: This bacteria normally inhabits the ______ of _____.  It enters the human skin via a _________ and elicits an ________ response at the inoculation site.  From here the bacteria can spread locally to _____ or ________.  The infection has the possibility to progress to _______.

This bacteria normally inhabits the oral cavity of animals.  It enters the human skin via a bite wound and elicits an inflammatory response at the inoculation site.  From here the bacteria can spread locally to soft tissue (cellulitis) and bone (osteomyelitis).  The infection has the possibility to progress to septicemia.

132

P. multocida dx 

Gram (-) coccobacilli with bipolar staining.

133

P. Multocida tx 

Suturing the wound may worsen the infection by creating a closed anaerobic environment which can favor bacterial growth. Penicillin G.  Clean and drain wound.

134

This is the only nonmotile Clostridium member.

Clostridium perfringens

135

necrosis of the small intestine caused by β-toxin release.  Common in New Guinea following large ingestion of pork (excess protein overwhelms trypsin digestion of β-toxin) 40% mortality.

Enteritis necroticans: caused by Clostridium perfrigens

136

C. perfringens clinical presenation

cellulitis, gas gangrene (myonecrosis with crepitus), food poisoning

137

C. perfringens pathology  -- Cellulitis

bacteria normally found in the ____ and _____.  Bacteria infect _____ environment of ________ and release _______ (_______ and _______).  This generates a ____ _______ infection and ______ production. The infection eventually forms collections of _____ under the skin that _____ when touched (______).

Cellulitis – bacteria normally found in the soil and GI tract.  Bacteria infect anaerobic environment of necrotic skin wound and release digestive enzymes (collagenase and hyaluronidase).  This generates a slow painless infection and gas production.  The infection eventually forms collections of gas under the skin that crackle when touched (crepitus).

138

C. perfringens Gas Gangrene Pathology

The infection is initiated from ____________ introduced into ____ _____ wounds. Here the spores can _____ and ______ in the ______ environment to release _______ which causes ________; _______ enzymes which produce ______ and _______.  Gangrenous muscles lead to ________ leaking from the skin. ________ may follow.

The infection is initiated from spores found in the soil.  These spores are introduced yet deep muscle wounds (military wounds, automobile accidents, crude abortions). Here the spores can germinate and grow in the anaerobic environment to release alpha toxin (lecithinase) which causes deep muscle cell necrosis; degradative enzymes which produce subcutaneous gas bubbles and crepitus.  Gangrenous muscles lead to black fluid exudate leaking from the skin. Shock may follow.

139

C. perfringens Food Poisoning pathology

Initiated from spores found in _____. These spores can survive _____ and germinate to __________ that is then _______. The bacteria release _______ in the ______.  This ______ inhibits ________ and damages the ______. This causes _______, ________, and ________. _____  and ______ are not common.

the infection is initiated from spores found in meat and poultry foods. These spores can survive cooking and germinate to contaminate food that is then ingested. The bacteria release heat-labile enterotoxin in the GI tract.  This enterotoxin inhibits glucose transport and damages the epithelium. This causes diarrhea, gastric pain, and nausea.   Fever and vomiting are not common.

140

C. perfringens Dx

Gram (+) rod, strict anaerobe, nonmotile.

141

C. perfringens Tx 

surgical removal of infected areas. Hyperbaric oxygen to kill anaerobic organisms. Penicillin, clindamycin (only effective in local, weak infections).

142

Trichinella spiralis clinical presentation

gastroenteritis, myalgia.

143

Trichinella spiralis pathology

Reservoir = ____.  ________ ingested from ________.  _____ mature into ______ in ________.   ______ mate and eggs mature to _____. ______ can penetrate _________ and gain access to ______ --> _________ and ______.

______ can be carried by ____ to ______ (often to ____, _____, _____, _____) where localized inflammation --> _______. ______ can form a ______  that can last for years and may calcify.

If many __________ are ingested this can lead to a severe infection where the _____ can migrate to the heart and brain causing ________ and ________.

Reservoir = pigs.  Encysted larvae ingested from uncooked meat.  Larvae mature into adults in small intestine.  Adult worms mate and eggs mature to larvae. Larvae can penetrate intestinal wall and gain access to bloodstream --> diarrhea, pain.

Larvae can be carried by blood to skeletal muscle (often to extraoculars, masseters, tongue, and diaphragm) where localized inflammation --> myalgia. Larvae can form a fibrous cyst that can last for years and may calcify.

If many encysted larvae are ingested this can lead to a severe infection where the larvae can migrate to the heart and brain causing myocarditis and encephalitis.

144

Trichinella spiralis dx

eosinophilia.  Striated muscle biopsy contain cysts with larvae.  Serology for chronic infection.

145

T. spiralis tx

Mebendazole/thiabendazole (against adult worms in the small intestine).  No treatment to remove cysts from muscle.  Steroids for severe myositis and myocarditis.

146

Taenia solium clinical presentation

intestinal infection – asymptomatic, malnutrition, abdominal discomfort.  Tissue infection – cysticerosis (neurological defects, blindness).

147

T. solium pathology: Intestinal infection

intestinal infection:  larvae found as ______ in _______ which get ingested in ________.  In the _________ the larvae mature and grow to generate adult worms consisting of a _________ and ________.  The ______ attaches to the ________, _______ containing eggs passed in ______.  The worm consumes the food that is ingested by the host leading to __________.

intestinal infection:  larvae found as cystercerci in pig muscle which get ingested in poorly cooked pork.  In the small intestine the larvae mature and grow to generate adult worms consisting of a scolex (head) and numerous proglotids (autonomous segments).  The scolex attaches to the intestinal wall, proglotids containing eggs passed in feces.  The worm consumes the food that is ingested by the host leading to malnutrition.

148

T. solium pathology: Tissue infection

humans ingest eggs from _________  and the eggs hatch into _____ in the _______.  ______ penetrate the _______ and travel to other tissues (________, _________ and __________) to form _______ containing ______.  The ________ grow slowly eventually leading to neurological defects (seizures, focal symptoms) or blindness.  When _____ die (several years later) this caused increased _______ and __________.

humans ingest eggs from infected feces and the eggs hatch into oncospheres in the small intestine.  Oncosheres penetrate the intestinal wall and travel to other tissues (brain, skeletal muscle, and eye) to form cysticerci containing larvae.  The cysts grow slowly eventually leading to neurological defects (seizures, focal symptoms) or blindness.  When cysts die (several years later) this caused increased inflammation and aggravated symptoms.

149

T. solium dx 

intestinal infection:  proglottids, eggs in stool.  

Tissue infection:  calcified cysticerci in muscle, brain on X-ray or CT scan.  Eosinophilia in muscle, brain also seen in X-ray or CT scan.

150

T. solium tx

intestinal infection:  niclosamide + cathartic; praziquantel.  

Tissue infection:  praziquantel or albendazole + steroids (reduce inflammation from the dying cysts).

151

152

Acute bacterial infection CBC w/ differential results

High WBC (>11,000), high PMNs (>60%), left shift (banded)

153

Both Staph aureus and strep pyogenes are ________ hemolytic

Beta

154

Treatment for osteomyelitis (suspect staph)

Possible draining of abscess, empiric abx - IV → clindamycin w/ or w/o ciprofloxacin, or levofloxacin

MRSA - Vancomycin

155

Staph aureus vs. epidermidis

Aureus - beta-hemolytic, yellow-like colonies, color change on mannitol salt agar

Epidermidis - common in IV infections, gamma-hemolytic, white colonies, no color change on mannitol salt agar

 

Both gram + cocci, catalase + 

Mannitol salt agar changes color from red to yellow in acidic

Both can grow in the salty area (like skin)

156

Most common microorganism in osteomyelitis in sickle cell

Salmonella typhi 

157

Salmonella produce oxidase?

No - Oxidase negative (many gram-negative rods DO produce oxidase, like pseudomonas)

158

Chronic Granulomatous Disease

Deficient NADPH oxidase - cannot make  enough H2O2 to kill catalase+ phagocytosed cells 

(usually cells make enough H2O2 to kill bacteria regardless of catalase, if deficient NADPH oxidase - catalase converts H202 to water and hydrogen - so if only have a little, not gonna work)

159

Following a barbecue hosted by a hunter who served “black bear burgers” several guests develop abdominal pain and diarrhea.  Their condition progresses about a week later to fever, myalgia, periorbital edema, and petechial hemorrhages in the conjunctiva.  A peripheral blood smear shows an increased eosinophil count.  What is the most likely cause of these symptoms?

Trichinosis

 

(parasites --> eosinophils = hallmark)

160