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ID Week 5 > ICL 2.23: Rickettsia & Coxiella > Flashcards

ICL 2.23: Rickettsia & Coxiella Flashcards

1
Q

what’s the microbiology of rickettsia?

A

gram (-) pleomorphic rods

obligate intracellular parasites = can’t make ATP!

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2
Q

what’s the microbiology of coxiella?

A

gram (-) pleomorphic = coccobacillus

obligate intracellular pathogen

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3
Q

do rickettsiaceae gram stain?

A

yes but not well because thin PG layer

giemsa is best for staining

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4
Q

how are rickettsiaceae transmitted?

A

arthropod vectors = ticks, mites, lice, and flease

most species are maintained in their arthropod hosts by transovarian transmission = don’t have to have a blood meal from humans to maintain bacteria

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5
Q

what disease does R. rickettsii cause? vector? host? location?

A

rocky mountain spotted fever

vector = ticks

hosts = small mammals, dogs, rabbits, birds

North & South America

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6
Q

what disease does R. akari cause? vector? host? location?

A

rickettsialpox

vector = mites

hosts = mice, rats

worldwide

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7
Q

what disease does R. prowazekii cause? vector? host? location?

A

epidemic typhus

vectors = human body lice –> hosts = humans

OR

vectors = lice, fleas –> hosts = flying squirrels

worldwide

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8
Q

what disease does R. typhi cause? vector? host? location?

A

endemic typhus

vector = fleas

hosts = opossums

USA

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9
Q

what disease does coxiella burnetii cause? vector? host? location?

A

Q fever

vector = ticks

hosts = small mammals, sheep, goats, cattle, dogs

worldwide

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10
Q

what disease does orientia tsutsugamushi cause? vector? host? location?

A

scrub typhus

vectors = mites

hosts = rodents

asia, india, australia

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11
Q

how do rickettsiae enter host cells?

A

they enter host cells by stimulating phagocytosis or endocytosis

after engulfment, these bacteria degrade the phagosomal membrane by using phospholipase

then the bacteria replicate in the cytoplasm or nucleus, and are continually released from the cell

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12
Q

how do rickettsiae move around in the host cell?

A

they have intracellular motility via actin polymerization!

**the exception is the typhus group

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13
Q

which of the following do NOT utilize actin polymerization to mediate intracellular motility within host cells?

A. typhus group rickettsia

B. spotted fever group ricettsia

C. burkholderia pseudomallei

D. listeria monocytogenes

E. shigella flexneri

A

A. typhus group rickettsia

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14
Q

which cells do rickettsiae invade? what happens?

A

endothelial cells

rickettsial diseases are model examples of vasculitis with localization in endothelial cells –> the bacteria then uses the actin “railroad” to punch through to the next cell without detection

the major pathophysiologic effect of endothelial cell injury is increased vascular permeability = edema, hypovolemia, hypotension, hypoalbuminemia

rickettsiae also routinely infect vascular smooth-muscle cells

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15
Q

which bacteria causes Rocky Mountain spotted fever?

A

rickettsia rickettsii

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16
Q

which cells does rickettsia rickettsii infect?

A

it infects the cells lining blood vessels throughout the body

damage causes the blood to leak via tiny holes into surrounding tissues = rash!!

because of this, severe manifestations of this disease may involve the respiratory system, central nervous system, gastrointestinal system, or renal system

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17
Q

what are some of the risk factors of R. rickettsii infection?

A
  1. age extremities (young or old)
  2. male
  3. AA and american indian race
  4. chronic alcohol abuse
  5. glucose 6-phosphate dehydrogenase deficiency (we don’t know why)
  6. frequent exposure to dogs and residing near wooded-high grass areas increases risk of infection
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18
Q

is the incidence of RMSF increasing or decreasing?

A

increasing….

we think it’s because people are living in areas with more ticks

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19
Q

what is the principal reservoir and vector for R. rickettsii?

A

infected hard ticks

  1. wood tick = west US
  2. dog tick = eastern US and california

just know that the ticks that cause RMSF in america are a different species than the ones in south america

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20
Q

how is R. rickettsii transmitted?

A

ticks transmit the organism to vertebrates primarily by their bite

but also, infection may occur after exposure to crushed tick tissues, fluids, or tick feces because it’s enough to get through your skin and infect you

however, the bite is more infectious

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21
Q

what are the stages of how a tick infects someone with R. rickettsii?

A

ticks can become infected from feeding on an infected host in either the larval, nymphal, or adult stage –>
the major mammalian reservoir is wild rodents

after developing into the next stage, R. rickettsii may be transmitted to a second host by either:

  1. during the subsequent feeding process
  2. male ticks may infect female ticks through body fluids or spermatozoa transfer
  3. female tick can also transmit R. rickettsii to her eggs = transovarial transmission

once infected, a tick can carry the pathogen for life

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22
Q

where are most cases of RMSF in the US?

A

the tick belt!!!

aka the south-Atlantic and south-central regions of the United States

recently, highest incidence rates were OK, NC, MO, TN, AR

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23
Q

where is RMSF in the world?

A

it’s a western hemisphere disease!

aka it’s only in the americas

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24
Q

what time of the year is RMSF most common?

A

the summer months!!

this is when people are out and about and tick exposure is higher

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25
Q

which age group has a higher incidence of RMSF?

A

elderly

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26
Q

are people hospitalized for RMSF?

A

hospitalization rates have decreased over the years due to out increased ability to identify the disease earlier

the number of U.S. cases has increased dramatically since 2000

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27
Q

in what populations is RMSF often fatal?

A

Increased risk of fatal outcome in ages 0-9 years, American Indians, and African-Americans

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28
Q

in which 5 states do most RMSF cases occur in the US?

A
  1. Arkansas
  2. Missouri
  3. NC
  4. oklahoma
  5. TN
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29
Q

what are the symptoms of RMSF?

A

DAYS 1-2
1. abrupt onset high fever

  1. headache
  2. myalgia
  3. malaise

DAYS 2-4
1. faint macular rash begins on wrists and ankles and spreads centrally

  1. abdominal pain, nausea/vomiting
  2. cough
  3. calf tenderness
  4. periorbital and peripheral edema (more common in kids)

DAYS 5-7
1. fever > 104

  1. worsening respiratory status
  2. worsening abdominal pain
  3. rash becomes petechial and widely spread; involves palms and soles of feet**

DAYS 7-9
1. rash becomes diffuse and forms purpura

  1. necrosis of digits (could need amputation)
  2. septic shock
  3. myocarditis and cardiac arrhythmias
  4. renal failure
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30
Q

what is the DOC to treat RMSF?

A

doxycycline

doxycycline is the most effective and preventing severe stages of illness and death if administered within the first 5 days of symptoms

fever usually subsides within 24-72 hours if treated within 4-5 days of symptoms

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31
Q

what kind of rash do you see with RMSF?

A

Most often begins as small, flat, pink, non-itchy spots (macules) on the wrists, forearms, and ankles

RASH STARTS ON THE EXTREMITIES AND MOVES TOWARDS TRUNK!!!

spots turn pale when pressure is applied and eventually can become raised on the skin

the characteristic petechial rash may not be obvious until the sixth day or later after onset of symptoms and it only occurs in 35-60% of people

**also the rash can involve the palms or soles which is not usual!

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32
Q

which of the following does NOT cause rashes on the palms of the hands?

A. coxsackie virus

B. primary syphilis

C. measles

D. staphylococcal toxic shock syndrome

E. neisseria meningitidis

A

C. measles

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33
Q

what are the symptoms of advanced/fatal cases of RMSF?

A

In advanced or fatal cases, purpura and skin necrosis or gangrene may develop

since the bacteria is infecting the blood vessels and causing damage, the tissues start dying because blood is leaking out of the vessels and causing the spots

could require amputation of necrotic tissue!!!

34
Q

what is the magic day for when you need to treat RMSF by?

A

5th day!!!

the odds of dying from RMSF are ≥5x greater for patients who do not receive anti-rickettsial therapy by the fifth day of their illness

must start treatment before diagnosis

35
Q

how do you diagnose RMSF?

A

so most of the following techniques are weak so it’s really more based on history and clinical symptoms because you need to act quick

  1. Weil-Felix test (crossreactive with proteus antigens)
  2. IFA to detect either IgM or IgG but the antibody would take a while to show up…
  3. PCR
  4. can’t really culture unless it’s in host cells since it’s a intracellular parasite
36
Q

how do you prevent RMSF?

A

no vaccine

avoiding tick exposure is best protection

37
Q

FLASHCARD: microbiology, pathology, epidemiology, clinical, diagnosis, and treatment of rickettsia rickettsii

A

MICROBIOLOGY: Gram – cocci, minimal peptidoglycan, will not Gram-stain, facultative anaerobe, actin-based motility, obligate intracellular growth, prefer endothelial cells

PATHOLOGY: After introduced into skin, stimulate endocytosis in endothelium. Replicate and use actin-polymerization to invade adjacent cells without exposure to extracellular immunity. Cause leakage from endothelium. Eventually spread all over body, causing leakage from endothelium in most organ systems

EPIDEMIOLOG: hosted and transmitted by Dermacenter ticks in North, Central, and South America. Transmitted transovarily from adult tick to egg (larvae). Major vertebrate hosts are rodents. Highest incidence in OK, NC, MO, TN, and AR, but seen throughout US. Most cases seen in Spring-Summer and increases with patient age. Severe outcome more common in young children, Native and African-American

CLINICAL: Become sick very quick. Initially develop high fever, severe headache, and general illness, but often do not associate tick-bite. Develop rash 2-6 days after fever begins, starting as macules on wrists, forearms, and ankles; includes palms and soles of feet. Eventually spread to other parts. If advances, see purpura, skin necrosis, and gangrene. Mortality rate from 20% to 70%. Treat quickly

DIAGNOSIS: Cannot culture on medium. Must diagnose quickly to start treatment. Initial diagnosis is on clinical symptoms and epidemiology. IFA detection of Rickettsial antibodies is the standard. Can also do IFA or PCR of skin tissues

TREATMENT: Rapid treatment with tetracyclines (doxycycline) is standard

38
Q

what disease does rickettsia akari cause and how is it transmitted?

A

causes Rickettsialpox

transmitted by mites

39
Q

describe the biphasic nature of rickettsia akari?

A

PHASE 1
red papule develops at site of mite bite –> after 1-2 weeks incubation papule develops an eschar (black wound) –> fever develops as bacteria spread systemically

PHASE 2
develop irregular fluctuating fever

headache, chills, rigors, profuse sweating, myalgias, and generalized rash

40
Q

how do you treat rickettsia akari infections?

A

doxycycline

low morbidity and mortality

41
Q

what is the causative agent of epidemic typhus?

A

rickettsia prowazekii

prowazekii = ePimedic

this is what killed most of Napolean’s army and soldiers in a bunch of other wars

42
Q

how is R. prowazekii transmitted?

A

epidemic typhus is a disease of humans*

human body lice transmits the agent from human to human

a person infested with infected lice acquires the bacteria when the lice or louse feces are rubbed into bite wounds or other skin abrasions

R. prowazekii is also endemic in flying squirrels –> fleas from squirrels can then feel on humans and infect them

43
Q

in what situations are you more likely to become infected with R. prowazekii?

A

epidemic typhus commonly occurs in cold climates where people live in overcrowded unsanitary conditions

ex. occur during war and natural disasters

typically facilitated by lice infestation

44
Q

in what areas of the world are R. prowazekii infections common?

A

epidemic typhus is currently prevalent in mountainous regions of Africa, South America, and Asia

45
Q

what are the symptoms of an R. prowazekii infection?

A

abrupt onset of symptoms

clinical manifestations of typhus include intense headache, chills, fever, and myalgia

characteristic rash develops on the fourth to seventh day of disease

if the disease progresses, you’ll see significant alterations of mental status like stupor or eventually coma

hypotension and renal failure are also common in severe disease

epidemic typhus is a life-threatening illness even for young, previously healthy persons: <40% fatal if untreated

46
Q

describe the rash spread seen in R. prowazekii infections

A

characteristic rash develops on the fourth to seventh day of disease

it first appears on the TRUNK and then spreads to extremities!! this is the OPPOSITE of RMSF!!!!

the rash also does NOT involve the face, palms or soles

47
Q

which cells does R. prowazekii infect?

A

endothelial cells (just like RMSF)

so it effects small venous, arterial, and capillary vessels

the organism proliferates and spreads to form multiorgan vasculitis

gangrene of the distal portions of the extremities may occur as a result of thrombosis of supplying blood vessels

48
Q

where does R. prowazekii replicate in the host cell?

A

the Typhus group does NOT utilize actin-based motility

it accumulate in cytoplasm until cell ruptures

49
Q

what is the causative agent of endemic typhus?

A

rickettsia typhi

50
Q

how is rickettsia typhii transmitted?

A

causes endemic typhus

rodents are natural reservoir

oriental rat flea and rat lice are vectors for human transmission

51
Q

where in the world are rickettsia typhii infections common?

A

occurs in most parts of the world, particularly in subtropical and temperate coastal regions

particularly common along coastal port regions

Temperate climates may have a rise in the flea vector and a subsequent rise in the incidence of murine typhus in the summer months

52
Q

is rickettsia typhii or rickettsia prowazekii more severe?

A

rickettsia prowazekii is more severe

rickettsia typhii has the same pathophysiology as epidemic typhus but it’s a milder disease

53
Q

what are the symptoms of a rickettsia typhi infection?

A

aka endemic typhus

after 1-2 weeks, see abrupt onset of fever and chills

rash spreading from trunk to extremities

the mortality rate for treated patients with murine typhus is 1-4%

severe disease in elderly/debilitated persons

54
Q

what is the causitive agent of scrub typhus?

A

orientia tsutsugamushi

55
Q

how is scrub typhus transmitted?

A

it’s caused by orientia tsutsugamushi bacteria

rodents and mites are the natural reservoirs

it’s transmitted to humans by larval mite bite

56
Q

where in the world in scrub typhus common?

A

Tsutsugamushi Triangle in Southeast Asia

current reemergence in locations such as India, Micronesia, and the Maldives

incidence is growing in South Korea and China north of the Yangtze River, where was previously unknown

57
Q

what are the symptoms of scrub typhus?

A

caused by orientia tsutsugamushi bacteria

black eschar forms at the site of chigger bite followed by spread through the lymphatics and blood

chills, fever, headache, abdominal pain, nausea and vomiting and muscle aches

can develop rash on trunk/axilla that spreads to rest of body but NOT on the palms or soles

58
Q

what happens in severe cases of scrub fever?

A

caused by orientia tsutsugamushi bacteria

  1. interstitial pneumonia
  2. acute respiratory distress syndrome
  3. meningoencephalitis
  4. acute kidney injury
  5. DIC
59
Q

how do you treat scrub fever?

A

doxycycline or azithromycin

60
Q

what is the causitive agent of Q fever?

A

coxiella burnetii

61
Q

what stain do you use for coxiella burnetii?

A

giemsa

it gram stains poorly

62
Q

how is coxiella burnetii transmitted?

A

wild animals are the natural reservoir but it’s best known for infecting farm animals (livestock)

ticks are an important vector for transmission between animals

however, aerosols are the main route of infection for humans –> vets and farmers are at risk

chronically infected animals shed bacteria in feces and urine, placenta, wool, milk

so people can get Q fever by touching feces, urine, milk or blood from an infected animal, breathing in bacteria, touching placenta or drinking raw milk

it’s also believed to be spread by wind = biochemical warfare??

63
Q

what are the two forms of the intracellular cycle of coxiella burnetii?

A
  1. small-cell variant (SCV) –> like the elementary body in chlamydia
  2. large-cell variant (LCV) –> like the reticulate body in chlamydia
64
Q

what is the small cell variant of coxiella burnetii?

A

metabolically inactive but infectious form of coxiella burnetii

it’s the extracellular form –> spore-like and extremely resistant to most environmental conditions

it attachs to the host cell membrane to enter phagocytic cells

after phagolysosomal formation, the drop in pH cause SCV to become active

SCV then divdes to become large-cell variant

65
Q

what is the large cell variant of coxiella burnetii?

A

metabolically active, replicating form of coxiella burnetii

intracellular form = protected from antibodies via location

it replicates until it receives the signal to begin forming SCVs

66
Q

how does coxiella burnetii spread throughout the body?

A

aerosols are the main route of infection for humans from livestock

after the SCV enter the lungs, the resulting LCVs proliferate and disseminate from the lungs to multiple organ systems

the bacteria persist in macrophages and use these to disseminate throughout host

67
Q

where in the US is Q fever common?

A

out west where there’s lots of livestock

68
Q

which age group is more susceptible to Q fever?

A

elderly

69
Q

what time of the year is Q fever common?

A

april-june

this is calf season!! and infected animals shed coxiella burnetii bacteria in their placenta!!!

70
Q

does Q fever require hospialization?

A

kinda….hospitalization rates are very high for Q fever

71
Q

what are the two types of Q fever that you can get?

A
  1. acute disease

2. chronic disease

72
Q

what are the symptoms of acute Q fever?

A

only about 50% of all people infected with C. burnetii show signs of clinical illness

after a long incubation period, most acute cases of Q fever begin with sudden onset of one or more of the following:

high fevers (up to 104-105° F), severe headache, general malaise, myalgia, confusion, sore throat, chills, sweats, non-productive cough, nausea, vomiting, diarrhea, abdominal pain, and chest pain

fever usually lasts for 1 to 2 weeks

30-50% of patients will develop an “atypical pneumonia”

hepatitis is also a common manifestation

most patients will resolve the infection within several months without any treatment

73
Q

what are the symptoms of chronic Q fever?

A

chronic Q fever is uncommon but is a much more serious disease –> characterized by infection that persists for more than 6 months

patients who had acute Q fever may develop the chronic form as soon as 1 year or as long as 20 years after initial infection

endocarditis is a serious complication of chronic Q fever

≥65% of persons with chronic Q fever may die of the disease

74
Q

how do you diagnose Q fever?

A

the symptoms of Q fever are not specific, so it is difficult to make an accurate diagnosis without appropriate laboratory testing

confirming a diagnosis of Q fever requires serologic testing to detect the presence of antibodies to Coxiella burnetii antigens

75
Q

how can you diagnose Q fever based on antigenic phases?

A

Phase I is the initial form found in infected animals, but LPS levels are low = highly infectious SCV form; smooth LPS

Phase II is expressed later after become less infectious, but at higher levels = LCV form; rough LPS

in acute Q fever, IgM levels to phase II is usually significantly higher than that to phase I

with chronic Q fever, antibodies to phase I antigens of C. burnetii generally require longer to appear and indicate continued exposure to the infectious form of bacteria

so during a chronic infections, high levels of IgG to phase I in later specimens in combination with constant or falling levels of phase II IgG antibodies indicate chronic Q fever

76
Q

how do you treat Q fever?

A

DOC = doxyclycline for adults and children of all ages

antibiotic treatment is most effective when initiated within first 3 days of illness

chronic Q fever endocarditis is much more difficult to treat effectively and often requires the use of multiple drugs = doxycycline and hydroxychloroquine in Q fever endocarditis for 18 months for native valves and 24 months for prosthetic valves

77
Q

how do you prevent Q fever?

A

vaccine exists but not available in america

since most outbreaks occur around livestock facilities, prevention and control efforts are usually directed primarily toward these environments. these include:

  1. appropriate disposal of placenta and other birth products
  2. release only pasteurized milk and milk products
  3. quarantine imported animals
78
Q

what are the symptoms of Q fever in animals?

A

C. burnetii does not usually cause disease in infected reservoir animals

however you will often see aborted offspring in pregnant animals

79
Q

how infectious is Q fever?

A

very….

the infectious dose of virulent Phase I organisms in laboratory animals has been calculated to be as small as a single organism

estimated human ID25-50 (inhalation) for Q fever is 10 organisms

it’s a BSL3 organism

80
Q

FLASHCARD: microbiology, pathology, epidemiology, clinical, diagnosis, treatment of coxiella burnetii

A

MICROBIOLOGY: Gram – cocci, will not Gram-stain, obligate intracellular parasite. Has two-phase life cycle. Small-cell variant (SCV) is infectious, non-metabolically active stable particle. Large-cell variant (LCV) not stable outside host cell, but replicate intracellular until form EB, then released

PATHOLOGY: SCV are very stable in the environment and can be spread in aerosols over a wide area. Enter lungs of susceptible animals/humans, where infect tissues and macrophages. Then convert to LCVs and replicate or persist in host cells. Can disseminate in host within macrophages. Non-reservoir hosts develop inflammatory disease in tissues where bacteria persist, including lungs, liver, and heart (severe)

EPIDEMIOLOGY: C. burnetii are found in the birth products (i.e. placenta, amniotic fluid), urine, feces, and milk of infected animals. People can get infected by breathing in dust that has been contaminated by these infected animal materials. Often transmitted between animal hosts via tick-bite. Most cases in Spring-early Summer and more prevalent in elderly. Most associated with interaction with livestock, particularly in western US

CLINICAL: About 50% of exposed will develop acute disease, with general illness symptoms. Severe cases may develop inflammation of the lungs (pneumonia) or liver (hepatitis). A small percentage of these may eventually develop chronic disease, most commonly those with heart valve disease, blood vessel abnormalities, or are immunosuppressed. Usually develop severe endocarditis

DIAGNOSIS: Cannot culture on plates. Usually test for antibodies to Phase I (early LPS) and Phase II (late LPS). In acute cases, IgM to Phase II is much higher than Phase I. In chronic disease, high levels of IgG to Phase I combined with similar or falling levels to Phase II

TREATMENT: Many acute cases self-resolve, but treatable with doxycycline. If chronic disease, treat with doxycycline and hydroxychloroquine for 18-24 months

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