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ID Week 5 > ICL 2.24: Zoonotic Bacterial Diseases > Flashcards

ICL 2.24: Zoonotic Bacterial Diseases Flashcards

1
Q

what’s the microbiology of bartonella?

A

gram (-) coccobacillus

aerobic

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2
Q

what’s the microbiology of ehrlichia?

A

gram (-) coccobacillus

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3
Q

what’s the microbiology of anaplasma?

A

gram (-) coccobacillus

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4
Q

which stain do you use for bartonella species?

A

gram stain poorly

instead do Warthin-Starry silver staining of lymph nodes/lesions

you’ll see brown to black coccobacilli against a pale yellow/amber background

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5
Q

in what media do you grow bartonella?

A

chocolate agar

hemin required

optimal growth at 34-37 C, 5% CO2

takes 14 days for colonies to grow though….

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6
Q

what’s the reservoir for bartonella?

A

animal and arthropod reservoirs

do not appear to cause disease in animal reservoir hosts, but do in other animals

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7
Q

how is bartonella transmitted?

A

different pathogenic species are transmitted by fleas, lice, or sandflies

NOT TICKS

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8
Q

which cells do bartonella infect?

A

RBCs or endothelial cells in human hosts

primary niche of bacterial colonization is believed to involve the vascular endothelium

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9
Q

what’s the unique effect that bartonella have on the body?

A

they cause vasoproliferative lesions = angiogenesis

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10
Q

what is the infection process of bartonella species?

A
  1. they colonize the vascular endothelium
  2. at five-day intervals, bacteria are released from the primary niche into the bloodstream

(bloodborne bacteria can reinfect the endothelium to start another infection cycle)

  1. bloodborne bacteria also bind to, invade, and replicate within RBCs

they specifically replicate in an intracellular membrane-bound compartment

  1. eventually, they stop replicating and persist within RBCs for several weeks

different Bartonella species reach different levels of bacteremia/RBC infection rates

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11
Q

how do Bartonella enter endothelial host cells?

A

dntry of Bartonella into endothelium is dependent on actin cytoskeleton

they bind to various extracellular matrix (ECM) components and membrane proteins

then single bacteria or small clusters are internalized in Bartonella-containing vacuoles (BCVs) but they stay right at the surface

it’s the injection of T4SS that interferes w/ internalization and allows bacterial clustering on surface

these clusters are surrounded by actin-rich protrusions of the host cell membrane and are eventually engulfed as large assemblies in invasome structures = looks like big bumps on cell surface EM

so the bacteria is finally taken up via the invasome!

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12
Q

how do Bartonella enter host RBCs?

A
  1. attachment mediated by T4SS or flagella
  2. small secreted deformation factor induces pits & trenches on RBC membrane
  3. dvaginations containing the bacteria pinch off into interior
  4. bartonella replicate in the RBC vacuole & persist there for the lifetime of RBC

this increases the likelihood for its spread through blood-feeding insects

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13
Q

how do Bartonella trigger vascular tumor formation?

A

vasoproliferative bartonellae adhere to and invade endothelial cells

they cause direct stimulation of endothelial cell proliferation and inhibition of apoptosis

they also trigger proinflammatory response that recruits macrophages and other leukocytes

at this point the bacteria produce angiogenic factor which causes the macrophages to make vascular endothelial growth factor (VEGF)

VEGF is potent stimulator of angiogenesis

“angiogenic factor” itself also directly stimulates blood vessel formation

then to top it all off, bacterial colonization/growth and macrophage activation results in hypoxic conditions which again, upregulates VEGF

all of this VEGF results in paracrine stimulation of endothelial cell proliferation

this whole combination of stuff mediates vascular tumor formation!!!! it looks like a kaposi sarcoma

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14
Q

what disease does bartonella henselae cause in immunocompetent vs. immunosuppressed people?

A

healthy people = cat scratch disease

immunocompromised people = bacillary angiomatosis (BA) or peliosis

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15
Q

what is the reservoir for bartonella henselae?

A

domestic cats! (sometimes dogs too)

50% of cats in the U.S. are infected at some point during their life span; especially kittens

cats are more likely to be infected in warm humid climates

infected animals usually are not sick

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16
Q

what are the 4 diseases that can be caused by bartonella henselae?

A
  1. cat scratch disease
  2. bacillary angiomatosis
  3. peliosis = vascular lesions in liver or spleen; not just on the skin like BA!
  4. endocarditis
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17
Q

what do the colonies of B. henselae look like on agar?

A

small white irregular colonies

all different sized circles

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18
Q

how is bartonella henselae transmitted?

A

cat to cat transmission is via flea bite

cat to human transmission is largely through direct contact/trauma = cat scratch, bite or even licking of wound

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19
Q

what are the symptoms of cat scratch disease?

A

caused by bartonella henslae

1 week after cat scratch you may see:

  1. papule or pustule at innoculation site
  2. fever
  3. tiredness
  4. headache

1-4 weeks later bacteria travel to nearby lymph nodes like armpit, groan or neck and lymph nodes will get really big and painful

in an immunocompetent person the infection is self-limiting and nodes usually shrink to normal size within weeks to months

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20
Q

do you develop protective immunity following cat scratch disease?

A

yup

antibodies produced during infection are subsequently protective

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21
Q

what are the possible complications associated with cat scratch disease?

A
  1. Parinaud’s oculoglandular syndrome

2. encephalitis/meningitis/myelitis

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22
Q

what is Parinaud’s oculoglandular syndrome?

A

possible complication of cat scratch disease which is caused by bartonella henslae

it’s a combination of conjunctivitis and local lymphadenopathy (big bulging lymph nodes) that usually happens when the scratch is near the head

can see necrosis, vasculitis, granulomatous inflammation and cococcobacilli will be present in lesions

there’s also proliferation/dilation of blood vessels

even with all these symptoms though there’s no pain and no discharge…

in fact, it usually resolves within 2-4 months with no sequelae

you just have to make sure it doesn’t progress to encephalitis/meningitis

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23
Q

describe encephalitis/meningitis associated with cat scratch disease

A

onset is sudden

fever, convulsion is often first presenting sign

children between 7-12 at risk

recovery is rapid (within 2-14 days), sequelae are rare

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24
Q

what is bacillary angiomatosis?

A

disease state of bartonella henslae exhibited by immunosuppressed patients

lesions are usually seen in skin, but may also manifest in bone, GI tract, reproductive tract, lymph node, and CNS

*bacteremic!! BA lesions form in several organ systems & mucosa

BA is more often caused by B. quintana and B. bacilliformis

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25
Q

what are the symptoms of bacillary angiomatosis?

A
  1. reddish vascular nodules, multiple lesions, tenderness

lesions are undistinguishable from that of Kaposi’s sarcoma

  1. fever, chills, malaise, headache, anorexia
  2. characterized by proliferation of vascular endothelial cells and neutrophils/bacteria scattered throughout lesion
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26
Q

how do you treat bacillary angiomatosis?

A

erythromycin

2-4 weeks or longer if needed

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27
Q

what is the host and vector of bartonella quintana?

A

only human hosts

lice vectors

no known animal vectors!

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28
Q

how is bartonella quintana transmitted?

A

body lice

B. quintana multiplies in the lice intestine and is transmitted to humans by feces through altered skin –> lice feed alot which provokes scratching and allows the lice feces filled with bacteria to enter!

poor personal hygiene conditions

most current cases are seen in homeless and/or chronic alcoholism

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29
Q

what do bartonella quintana infections cause in immunocompetent patients?

A
  1. trench fever
  2. endocarditis
  3. chronic bacteremia
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30
Q

what do bartonella quintana infections cause in immunocompromised patients?

A

bacillary angiomatosis

it’s actually associates more with bone/subcutaneous than BA caused by B. henselae

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31
Q

what are the symptoms of trench fever?

A

caused by bartonella quintana

sudden onset of severe headache, pain in the shin bones, elevated temperature

may also see fatigue, restlessness, dizziness, macular truncal rash, NVD, splenomegaly

between days 3-7, the temperature would suddenly drop to normal

then you’d see recurrence of ~5 day cycle, with each attack being less severe

trench fever often results in prolonged disability but no fatalities reported

“quintana” = occuring every 5 days!

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32
Q

what disease does bartonella baciliformis cause?

A

Carrion’s disease = Oroya fever + verruga peruana

33
Q

what is Carrion’s disease?

A

caused by bartonella baciliformis

a biphasic disease that is endemic in the valleys of the South American Andes

consists of both the Oroya fever = phase 1 and verruga peruana = phase 2

34
Q

how is Carrion’s disease transmitted?

A

caused by bartonella baciliformis

transmitted by the sandfly (Phlebotomus verracarum)

no known animal reservoir

35
Q

what are the two phases of Carrion’s disease? what happens during them?

A

PHASE 1 = Oroya fever (acute)

highly fatal febrile anemia

fever, headache, pain in the shins, splenomegaly

caused by massive invasion and lysis of RBCs from a hemolysin that B. bacilliformis produces (other bartonella species don’t produce it)

PHASE 2 = Verruga peruana (chronic)

if you survive oroya fever, the disease will progress to chronic secondary phase of verruga peruana

the bacteria colonize the vascular endothelium and cause vasoproliferative eruptions of the skin = verruga

these lesions are identical to BA lesions caused by B. henselae and B. quintana but they’re limited to the skin

they develop within 1-2 months & persist months to years

it correlates with development of humoral response

36
Q

how do you treat B. henselae infections?

A

Cat scratch disease = antibiotic treatment not recommended

bacillary angiomatosis = erythromycin or tetracycline; 2-3 months

37
Q

how do you treat B. quintana infections?

A

doxycycline for 4 weeks plus gentamicin for 2 weeks

38
Q

how do you treat B. bacilliforimis infections?

A

erythromycin, doxycycline, ciprofloxicin; 1-2 week

39
Q

how do you diagnose bartonella infections?

A

diagnosis is hard and you often have to use symptoms, history and geography

so like evidence of cat scratch/bite (CSD, BA), trip to South America (Carrion’s disease), poor living conditions (trench fever) are important for diagnosis

serologic tests like ELISA are msot practical for diagnosis but they’re only effective after humoral response has occurred

you can’t culture this bacteria!!!

40
Q

FLASHCARD: microbiology, pathology, epidemiology, clinical, diagnosis and treatment of bartonella

A

MICROBIOLOGY: Curved, pleomorphic Gram – bacillus, poor Gram strain (Warthin-Starry in tissues), fastidious growth (use chocolate agar for 14 days), infect erythrocytes and endothelial cells in humans, different species transmitted by different arthropod vectors

PATHOLOGY: Infects endothelial cells after introduced into skin by vector (B.h.-flea, B.q.-human louse, B.b.-sandfly). Released at intervals into bloodstream to infect erythrocytes (RBCs). Disease severity is related to relative ability of each strain to achieve high numbers in blood and/or lyse RBCs; B.h. is mild, B.q. is moderate, and B.b. is severe

EPIDEMIOLOGY: B.h. is found in more temperate zones and associated with animal-transmission via fleas or biting/scratching. Mainly transmitted to human via cat-scratch, and most cases are children. B.q. is only transmitted via louse, so seen in areas with poor hygiene or war-associated populations. B.b. is only found in valleys of Andes mountains, where transmitted via bite of sandfly

CLINICAL: Cat scratch disease (B.h.) is usually mild and self-limiting, with swollen lymph nodes; however, immunosuppressed can develop more severe disease and vascular tumors (bacillary angioedema). Trench fever (B.q.) exhibits a “Quintana”, where every ~5 days see onset of severe headache, pain in shin bones, and elevated temperature that lasts 3-7 days, followed by ~5 days normal; debilitating, but not fatal. B.b. cause two disease: Oroya fever (acute) has massive invasion & lysis of RBCs, fever, headache, shin pain. Splenomegaly; highly fatal febrile anemia. Second is verruga peruana (chronic) where form large numbers of vascular tumors (bacillary angioedema)

DIAGNOSIS: Mainly diagnose by symptoms and epidemiology for each. Culture is impractical. Can stain lesions (Wartin-Starry) or test for antibodies for each bacteria. Treat Oroya fever ASAP!

TREATMENT: CSD is usually self-limited. DOC is doxycycline, or erythromycin

41
Q

which genuses are in the anaplasmataceae family?

A
  1. anaplasma
  2. ehrlichia
  3. neorickettsia
  4. wolbachia
42
Q

which bacteria cause human ehrlichioses?

A
  1. Ehrlichia chaffeensis**
  2. Ehrlichia ewingii
  3. Anaplasma phagocytophilum**
  4. Neorickettsia sennetsu

all of these are in the anaplasmataceae family

43
Q

what is the microbiology of anaplasmataceae family?

A

gram (-) cocci

obligate intracellular pathogens = can’t grow them on media outside of a cell

lack LPS and peptidoglycan*

44
Q

how are anaplasmataceae family bacteria transmitted?

A

all transmitted by ticks

45
Q

what cell type do anaplasmataceae family bacteria infect?

A

they infect different leukocyte populations

they remain in phagocytic vacuoles and prevent fusion with lysosome

then they divide to form vacuole-bound colonies known as morulae –> a single cell can havae 3-15 morulae

**morulae are diagnostic for anaplasmataceae infection!!

they look like little spots inside neutrophils

46
Q

how are Ehrlichia chaffeensis and Anaplasma phagocytophilum transmitted?

A

Wild rodents are reservoirs for A. phagocytophilum

deer are reservoirs for E. chaffeensis (yellow)

each bacteria are usually transmitted to humans by the bite of infected ticks that have acquired the infection by taking a blood meal from respective reservoir wild animals

A. phagocytophilum and E. chaffeensis infect primarily granulocytes and monocytes, respectively

these infected leukocytes circulate throughout the body to cause systemic diseases

human brain infection is rare, but E. chaffeensis has been observed in human cerebrospinal fluid mononuclear cells

47
Q

which cells do Anaplasma phagocytophilum infect?

A

granulocytes = neutrophils, basophils, eosinophils

48
Q

which cells do Ehrlichia chaffeensis infect?

A

monocytes

49
Q

what is a marker for cell death?

A

elevated aminotransferase levels

50
Q

what disease does ehrlichia chaffeensis cause?

A

human monocytic ehrlichiosis (HME)

51
Q

what disease does anaplasma phagocytophilum cause?

A
  1. human granulocytic anaplasmosis (HGA)

2. tick borne fever

52
Q

what are the symptoms of HGA?

A

HGA = human granulocytic anaplasmosis which is caused by anaplasma phagocytophilum

  1. fever, chills, malaise
  2. thombocytopenia
  3. elevated aminotransferase
  4. rash, circular skin lesion
  5. intracytoplasmic inclusions in neutrophils
53
Q

where in the US are anaplasma phagocytophilum infections most common?

A

they cause human granulocytic anaplasmosis

areas where HGA may occur is based on distribution of vector tick species = ixodes scapularis

this distribution is consistent with the fact that the vector of HGA also transmits Borrelia burgdorferi = often see co-infection

most of the recognized HGA cases have originated from states that also have a high incidence of Lyme disease = Connecticut, Massachusetts, New York, Minnesota, and Wisconsin

in the western United States, the HGA agent is transmitted by the western blacklegged tick = ixodes pacificus

54
Q

which age group is more susceptible to anaplasma phagocytophilum infections?

A

elderly

55
Q

what are the symptoms of HME?

A

HME = human monocytic ehrlichiosis which is caused by ehrlichia chaffeensis bacteria

it’s called chaffeensis because it was first seen at fort chaffee during boot camp

fever, headache, pharyngitis, nausea, vomiting & dehydration 3 days after onset

PE revealed prominent cervical lymphadenopathy, splenomegaly, and no rash

CBC showed significant left shift = lots of immature cells = active infection

56
Q

how is ehrlichia chaffeensis transmitted?

A

lone star tick = western US

NOT efficiently transmitted to egg; larvae have to feed on an infected deer

disease distribution directly correlates with the geographic distribution of the Lone Star tick

57
Q

where are ehrlichia chaffeensis often seen in the US?

A

Arkansas, Missouri, Oklahoma, North Carolina, South Carolina, and Georgia

58
Q

what is the reservoir of ehrlichia chaffeensis?

A

deer

but can also be found in dogs, foxes, coyotes, wolves, raccoons, opossums, goats, and mice

vector = lone star tick

59
Q

what are the similarities between HME and HGA disease?

A

HME = caused by ehrlichia chaffeensis; infects monocytes/macrophages

HGA = caused by anaplasma phagocytophilum; infects granulocytes

symptoms appear 1-21 days after infection (tick-bite)

most common symptoms are fever, headache, chills, muscle aches and pains, fatigue, and malaise

rash is infrequent (more common for HME)

common clinical findings are thrombocytopenia (71%), leukopenia (49%), anemia (37%), and elevated hepatic transaminase levels (71%)

60
Q

what are the effects on the immune system that HME and HGA have?

A

HME infects monocytes while HGA infects granulocytes so the immune system is adversely affected due to infection and killing of leukocytes

this lessens the ability to fight other infections so you see many complications and getting sick from other diseases

61
Q

is HME or HGA more deadly?

A

Hospitalization is required for 50% of symptomatic patients with both diseases

but HME mortality rate is higher

rates higher in elderly

62
Q

how do E. chaffeensis and A. phagocytophilum infect cells?

A

they infect different cell types but they both:

bind to surface receptors that promote non-inflammatory uptake

then they’re both internalized into endosome but do not fuse with lysosome

they replicate within endosomal vacuole to form morulae

63
Q

what virulence factors do E. chaffeensis and A. phagocytophilum have?

A

both bacteria lack LPS and peptidoglycan

so they do not elicit a strong initial inflammatory response

they also downregulate ROI in monocytes and granulocytes, respectively

plus both can inhibit apoptosis of respective host cell types

64
Q

describe the biphasic life cycle of E. chaffeensis and A. phagocytophilum

A

kind of like chlamydia!!

initially, small dense-cored cells bind to host cells, are internalized and develop into large reticulate cells = EB

reticulate cells then mature into dense-cored cells or compact into clumps = RB –> formation of morulae!!

65
Q

which of the following have two different cell phases during their normal life cycle?

A. orientia tsutsumagushi

B. rickettsia rickettsi

C. neisseria gonorrheae

D. coxiella burnettii

E. bacillus anthracis

A

D. coxiella burnettii

66
Q

how do diagnose HME and HGA?

A

indirect immunofluorescence assay (IFA) is generally considered the reference standard but it takes a while for antibodies to develop….

PCR is the most rapid and specific diagnostic assay for HME and HGA

E. chaffeensis and A. phagocytophilum can only be cultured in host cells

base treatment on epidemiologic and clinical clues = tick exposure, fever, general malaise (sometimes see variable rash, but not diagnostic), thrombocytopenia, decrease in lymphocytes, increased aminotransferase levels, anemia

morulae are only detected in blood smears in 60% of patients but if they’re there they are diagnostic!

67
Q

how do you treat HME and HGA?

A

doxycycline!

68
Q

how do you prevent HME and HGA?

A

no vaccine

so just avoid tick exposure

69
Q

FLASHCARD: microbiology, pathology, epidemiology, clinical, diagnosis, and treatment of Ehrlichia chaffeensis & Anaplasma phagocytophilum

A

MICROBIOLOGY: Gram – coccobacilli, lack LPS & peptidoglycan, will not Gram-stain, obligate growth within either monocytes (E.c.) or neutrophils (A.p.) for growth/persist within morulae. Appear to have 2 forms, with inert small elementary body that infects host cell, then transform into larger reticulate body that multiplies within morulae before transform back to elementary body for release.

PATHOLOGY: After introduced into skin via tick-bite, migrate to bloodstream to infect either macrophages or neutrophils. Eventually cause reduction in these WBC, result in suppressed immunity. Can go on the infect multiple organs.

EPIDEMIOLOGY: E.c. is hosted/transmitted by Amblyomma americanum (Lone star tick) and A.p. by Ixodes ticks, and thus disease is only acquired within their ranges. Disease is more common in Spring-Summer, in males, and in elderly patients.

CLINICAL: E.c. (Human monocytic ehrlichiosis; HME) and A.p. (Human granulocytic ehrlichiosis; HGE) cause similar disease. After incubation of 1-2 weeks, become sick very quick. Most commonly see high fever, severe headache, fever, malaise, thrombocytopenia, and general illness, but often do not associate tick-bite. Rash is rare, but can occur. Commonly can lead to hospitalization. Fatal outcome is low if treat rapidly.

DIAGNOSIS: Difficult to diagnose. Cannot culture on medium. Initial diagnosis is on clinical symptoms and epidemiology. May be able to detect morulae within monocytes or neutrophils in blood smear. Eventually can detect antibodies in blood or PCR on blood cells. Ixodes ticks carry multiple pathogens (e.g. Borrelia, Babesia, Powassan virus), so should consider all options.

TREATMENT: DOC is tetracyclines (doxycycline)

70
Q

what is the microbiology of babesiosis microti?

A

trick question

they are eukaryotic parasites, NOT a bacteria

71
Q

how is babesiosis microti transmitted?

A

blacklegged tick = ixodesscapularis

same tick vector as B. burgdorferi and A. phagocytophilum

so an individual tick can carry and transmit any combination of these 3 pathogens

72
Q

where are babesiosis microti infections seen in the US?

A

geographic distribution and seasonality is same as Lyme disease and Anaplasmosis

most U.S. cases are B. microti and seen in upper Midwest and Northeast U.S.

recent increase in Babesiosis most likely due to the expansion of the white-tailed deer population in endemic regions –> deer do not carry infection, just provide blood meal for ticks

73
Q

what is the lifecycle of babesia microti?

A
  1. tick takes a blood meal from mouse
  2. diploid turns into gamete form in the mouse and then the tick takes another blood meal and ingests gametes
  3. fertilization in gut
  4. ookinete enters salivary gland
  5. tick bites human and sporozoites are introduced into host
  6. can be transmitted between humans via blood transfusion
74
Q

what are the symptoms of babesiosis?

A

most patients develop non-specific symptoms 1-4 weeks after inoculation

intermittent fever, fatigue, malaise, headache, chills, sweats, myalgia

babesia causes lysis of RBCs so you often see splenomegaly, hemolytic anemia, lymphopenia, thrombocytopenia, elevated serum lactate dehydrogenase, and elevated RBC sedimentation rate

symptoms last for week to months (or longer) if untreated, but usually resolves

however, patients with complicating conditions can have severe or fatal disease

75
Q

how do you prevent babesia microti infections?

A

no vaccine

avoid tick exposure

76
Q

how do you diagnose babesiosis?

A

definitive initial test is Giemsa or Wright stain of thin blood smears – babesia too small to see on thick smear

PCR can be performed, if available

antibodies can be detected by IFA or immunoblot

if tests are negative & symptoms persist, can inject patient blood into small rodent

77
Q

when should you consider babesiosis?

A

Residence/travel in endemic area

Received recent blood transfusion

Should be considered in patient with Lyme disease or HGA diagnosis since all pathogens are carried by the same tick co-infection is common

78
Q

what do babesia look like on a thin blood smear?

A

you can see tetrads of replicating merozoites arranged in a cross-like pattern

maltese cross is diagnostic!

79
Q

how do you treat babesiosis?

A

two combination options, both are great

  1. atovaquone + azithromycin
  2. clindamycin + quinine

7-10 days or 6 weeks if persistent relapsing infection

ID Week 5 (13 decks)

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