Dermatologic Manifestations of Bacterial Infections Flashcards

1
Q

What are the bacteria that cause rashes?

A
  • Neisseria meningitidis*
  • Staphylococcus aureus*
  • Rickettsia rickettsii*
  • Ehrlichia cheffeensis*
  • Anaplasma phagocytophilum*
  • Bartonella spp.*
  • Borrelia burghodorferi*
  • Treponema pallidum*
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2
Q

What are the Neisseria species that leads to skin manifestations?

A

Gram-negative diplococci

  • N. meningitidis*
  • N. gonorrhoeae*
  • Moraxella catarrhalis*
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3
Q

general features of Neisseria meningitidis

A

five major serogroups - A, B, C, W-135, Y

  • B, C, and Y are common in the US
  • serogroup A causes major epidemics in sub-Saharan Africa, China, and South America

in the U.S., most disease is sporadic or occurs as part of small epidemics (college campuses, day-care center, etc.)

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4
Q

Neisseria meningitidis determinants of pathology

A

endotoxin

pili - antigenic variation and may avoid recognition by the immune system in this manner

polysaccharide capsule - resists phagocytosis and complement-mediated killing, antibodies to the capsule confer immunity

surface receptors that bind and remove iron from transferrin and lactoferrin

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5
Q

What are factors that help fight N. meningitidis infections?

A

carriage of this organism in the upper respiratory tract is at about 10% of the general population - not sure why these people are resistant

antibodies to the capsule confer immunity

complement is important in host resistance to N. meningitidis, particularly the terminal complement component (C5-C9)

individuals lacking functional spleens are more susceptible

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6
Q

What are the clinical disease of Neisseria meningitidis infection?

A

meningococcemia

meningitis

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7
Q

meningococcemia

A

caused by N. meningitidis

sudden onset of fever, chills, nausea, vomiting, rash (diagnostic), myalgia and arthralgias

rash may be maculopapular, petechial, or ecchymotic

in fulminant disease, patients present with a very rapidly progressive illness characterized by shock, disseminated intravascular coagulation, and multiple-organ failure

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8
Q

meningitis

A

caused by N. meningitidis

associated with meningococcemia

severe headache, confusion, lethargy, vomiting

leads to coma, seizures, and focal neurologic signs

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9
Q

What are the diagnostic laboratory tests for Neisseria meningitidis?

A

gram-negative diplococci can usually be seen in samples of cerebral spinal fluid

culture of blood or CSF samples

counterimmunoelectrophoresis or latex agglutination assays (can detect live or dead organisms and can be useful even after antibiotic treatment)

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10
Q

What is the treatment of a Neisseria meningitidis?

A

penicilin G

resistant isolates have been reported with increasing frequency

cephalosporins (ceftriaxone) are also very active

chloramphenicol should be used in patients with severe penicillin allergies

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11
Q

What is the prevention of Neisseria meningitidis?

A

MCV4 - meningococcal conjugate vaccine (menactra) - capsular polysacchries conjugated to diptheria toxin (ages 2-55)

MPSV4 - meningococal polysaccharide vaccine (menomune) - capsular polysaccharides without conjugate, and protection is about 3 years

prophylatic rifampin or ciprofloxacin

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12
Q

What are the skin manifestations of Staphylococcus aureus?

A

toxic shock syndrome - blanching erythematous rash, hypotension or shock, organ failure, high fever, vomiting, diarrhea, sore throat, muscle pain

dequamation of skin after resolution

tampon use or infected wounds

TSST-1 or endotoxin

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13
Q

general features of Rickettsia rickettsii

A

gram-negative rod

obligate intracellular pathogen - requires host cell nucleotide cofactors and ATP to multiply

cause of Rocky mountain spotted fever (RMSF) - most common in the central and mid-atlantic states

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14
Q

What are the determinants of pathogenicity for Rickettsia rickettsii?

A

transmitted through tick bites (American dog tick and Rocky Mountain wood tick)

disseminate via lymphatics and bloodstream

OmpA to attach to endothelial cells

induces its own engulfment by endothelial cells and subsequent escape from vacuole into the cytoplasm

multiples in cytoplasm

uses host action to propel itself through cytoplasm and spread

endothelial cells are eventually killed and leads to increase vascula permeability, edema, and hemorrhage

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15
Q

What is the clinical disease of Rickettsia rickettsii?

A

Rocky Mountain Spotted Fever (RMSF)

fever, headache, mailaise, myalgia, nausea, and vomiting

after a few days, a macular rash develops - starts from wrists and ankles and subsequently spreads to the rest of the body, evolves over several horus or days to petechiae

vascular damage can lead to edema

disseminated intravascular coagulation, thrombocytopenia, shock and organ failure may develop if not promptly treated

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16
Q

What are the diagnostic laboratory tests for Rickettsia rickettsii?

A

takes up gram stain poorly - best visualized by Giemsa stain

culture is difficult and hazardous to laboratory personnel

serological tests require both acute and convalescent sera, most patients will have negative titers at the time of presentation

immunohistologic examination of a cutaneous biopsy of a rash lesion

PCR

treatment should not be withheld while wiating for results

17
Q

What is the treatment for Rickettsia rickettsii?

A

doxycyclin is the drug of choice

chloramphenicol is alternative - doxycycline allery and pregnant women

18
Q

What is the prevention of Rickettsia rickettsii?

A

avoidance of tick bites

19
Q

What are the general features of Ehrlichia chaffeensis?

A

causes erlichiosis - transmitted by tick bite (Lone Star tick)

infects monocytes and macrophages

presents with fever, headaches, myalgias, thrombocytopenia, and leukopenia

only a minority of patients (30%) develop a rash

organisms can be seen inside leukocytes as “mulberry”-like clusters called morulae

PCR diagnosis

20
Q

What are the general features of Anaplasma phagocytophilum?

A

causes anaplasmosis

infects neutrophils

transmitted by tick bite (Ixodes scapularis)

clinically, causes disease similar to Ehrlichiosis

organism forms morulae inside neutrophils

21
Q

What are the two medicall important Bartonella spp.?

A
  • B. henselae*
  • B. quintana*
22
Q

What are the general features of Bartonella spp.

A

tiny gram-negative bacilli that invade the endothelial cells and erythrocytes

NOT obligate intracellular bacteria but are discussed here beause they were formerly classified as Rickettsiaceae

16S ribosomal sequencing shows that they are not obligate intracellular

23
Q

What disease is called by Bartonella spp.?

A

bacillary angiomatosis

seen in immunocompromised invidiuals (especially those with AIDS)

vascular skin lesions that often resemble Kaposi’s sarcoma

may disseminate to almost any organ

cat-scratch disease

B. henselae -> an enlargement of one or more lymph nodes following a cat scratch or bite

24
Q

What are the general features of Borrelia burgdorferi?

A

spirochete

microaerophilic (grows best in presence of lower levels of oxygen)

three main loci of endemicity - Northeast, Centra, and Pacific Coast

25
Q

What are the determinants of pathogenicity of Borrelia burgdorferi?

A

colonizes ticks - Ixodes scaplaris in the northeast and central regions, and I. pacificus in the Pacific Coast

infects humans when tick takes blood meal

outer surface proteins (Osp) A and B - plasma encoded and primarilly expressed in the tick

OspC - upregulated during tick feeding and function is unclear but thought to allow bacteria to persist in very different environments

doe snot use iron! (use zinc and manganese instead)

26
Q

What is the early infection (stage 1) of Borrelia burgdorferi infection?

A

erythema migrans - anular erythematous rash that expands outward and has central clearing

occurs at site of the bite

due to the cutaneous spread of the organism outward from the site of inoculation

27
Q

What is the early infection (stage 2) stage of Borrelia burdorferi infection?

A

within days to weeks after the onset of EM, the organisms disseminate into the blood

arthralgias, fever, chills, malaise, meningitis, and cranial nerve palsies (paralysis)

cardiac involvement in the form of arrhythmias

28
Q

What is the lat infection (stage 3) stage of Borrelia burgdorferi infections?

A

months after infection

arthritis

encephalopathy (memory impairment, mood disturbance, or neuropathies)

29
Q

What are the diagnostic laboratory tests for Borrelia burgdorferi?

A

recognition of a characteristic clinical picture

confirmed by serologic testing - ELISA with confirmatory western blottting

gram-negative, but most easily visualized by Giemsa, Wright, or acridine orange stains

difficult to grow in culture

30
Q

What is the treatment for Borrelia burgdorferi?

A

early disease and arthritis - oral doxycycline or amoxicillin

neurologic abnormalities and cardiac involvement (IV ceftriaxone)

31
Q

What is the prevention of Borrelia burgdorferi?

A

a vaccine consisting of recombinant OspA

was withdrawnin 2002 due to poor sales and concern about safety

32
Q

general features of Treponema pallidum

A

spirochete

cause of syphilis

primary syphilic is associated with a chancre

secondary syphilis is associated with generalized lymphadenopathy and rash