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ID Week 3 > ICL 2.11: Borrelia & Leptospira > Flashcards

ICL 2.11: Borrelia & Leptospira Flashcards

1
Q

what is the microbiology of borellia?

A

spirochete

nontoxic, highly invasive, damage from immune system

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2
Q

what is the microbiology of leptospira?

A

spirochete

nontoxic, highly invasive, damage from immune system

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3
Q

what three bacteria are spirochetes?

A
  1. borrelia
  2. treponema
  3. leptospira
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4
Q

lyme disease vingette

A

no localizing symptoms

vomiting, nausea, aches, malaise, slight fever

eventually starts to feel better but large bullseye rash develops

walking through tall grass

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5
Q

which bacteria causes lyme disease?

A

borrelia burgdorferi

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6
Q

what are the structural features of borrelia burgdorferi?

A

OUTSIDE
1. outer membrane

contains few proteins in OM; majority of those are lipoproteins

  1. endoflagella*
  2. peptidoglycan
  3. inner membrane
    INSIDE

NO LPS
NO lipid A
NO lipoteicocic acid

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7
Q

what are the structural features of gram - bacteria?

A
  1. outer membrane
    LPS

porins and other surface proteins

  1. PG
  2. periplasm
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8
Q

what are the structural features of gram + bacteria?

A

no outer membrane

  1. thick PG
  2. lipoteicoic acid
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9
Q

during what time of the year is Lyme disease most common?

A

risk of human infection is greatest in late spring and summer

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10
Q

what are the 4 stages of tick growth?

A
  1. eggs
  2. larva
  3. nymph
  4. adults
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11
Q

how do ticks become infected with borrelia burgdorferi?

A

no transovarial transmission of B burgdorferi between parent ticks to their offspring so tick larvae are initially uninfected

but then naive larvae feed on infected mice and will sustain infection through molts to nymph and adult stages and therefore can transmit infection = persistence

nyph ticks then transmit infection to naive mice or humans – this allows maintenance of spirochete pool in wild

adult ticks then feed on deer and lay eggs

deer are not reservoirs for spirochetes, but provide blood meal that allows maintenance of tick population – so the number of Lyme cases correlates with acorn and deer population!

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12
Q

which tick species transmits Lyme disease?

A

Ixodes scapularis = eastern USA

Ixodes pacificus = california

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13
Q

what populations are most susceptible to Lyme disease?

A

most prevalent in the young (4-15; especially boys) and the elderly (45-85)

this is due to lack of proper tick surveillance

also in europe and asia and northeast america

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14
Q

which stage of tick usually transmits Lyme disease?

A

usually transmitted by nymph ticks

> 50% will never notice attached tick or remember bite

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15
Q

what are the risk factors for Lyme disease?

A
  1. presence of ticks known to harbor B. burgdorferi
  2. presence of mammalian/bird hosts to maintain B. burgdorferi reservoir = small rodents, migratory birds
  3. large terminal blood meal to maintain large tick population = deer
  4. proximity of humans and deer population (ticks)
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16
Q

what are the stages of Lyme disease?

A
  1. early disease = stage 1, primary

2. large disease = stage 2, subacute

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17
Q

what happens during the early stage of lyme disease?

A
  1. diagnostic symptom is erythema migrans = expanding bullseye rash at site of bite (70-80%)

may not be seen due to location of bite but believed to represent an inflammatory response to disseminating spirochetes

may be misdiagnosed in absence of erythema migrans

  1. “flu-like” symptoms: fatigue, malaise, fever, headache; no respiratory complications
  2. symptoms may occur days to weeks after infection

if diagnosed and treated appropriately, >99% are cured

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18
Q

what happens during the late stage of lyme disease?

A

occurs from weeks to years after initial infection once spirochetes disseminate to varied organs and tissues

most common complications are arthritis (60%), neurologic (20%) and cardiac (8%)

spirochetes are present in affected tissues

antiobiotics eventually resolve disease

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19
Q

how can you differentiate lyme disease from autoimmune arthritis?

A

pathology of Lyme arthritis is distinct from autoimmune arthritis because it can occur in the absence of B and T lymphocytes

the arthritis reflects the host inflammatory response to B. burgdorferi lipoproteins

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20
Q

what is causing arthritis in Lyme disease?

A

the arthritis reflects the host inflammatory response to B. burgdorferi lipoproteins

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21
Q

what are the clinical manifestations of confirmed lyme disease?

A
  1. erythema migrans (71%)
  2. arthritis (28%)
  3. facial palsy
  4. radiculoneuropathy (4%)
  5. meningitis/encephalitis
  6. carditis
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22
Q

what is radiculopathy?

A

a problem in which one or more nerves are affected and do not work properly

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23
Q

what is facial palsy?

A

characterised by facial drooping on the affected half, due to malfunction of the facial nerve (VII cranial nerve), which controls the muscles of the face

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24
Q

what are the neurologic complications that can happen with Lyme disease?

A
  1. Bell’s palsy = paralysis of facial nerve

usually resolves with antibiotic treatment

  1. lymphocytic meningitis
  2. radiculoneuritis
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25
Q

what are the cardiac complications that can happen with Lyme disease?

A
  1. atrioventricular block
  2. myocarditis
  3. palpitations
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26
Q

what is atrioventricular block?

A

one of the cardiac complications associated with Lyme disease

it’s when there’s interferance with the normal movement of
electrical signals from the heart’s
upper to lower chambers

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27
Q

what is acrodermatitis chronica atrophicans?

A

happens during late stage of european lyme borreliosis; predominantly seen in infections with Borrelia afzelii

it’s progressive fibrosing skin process that’s most evident on extremities – hard to diagnose

the pathophysiology is not understood but ACA develops after spirochetes persist for an extended period

but you don’t see spontaneous remission like other sequella

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28
Q

what happens if you don’t treat Lyme disease?

A

if left untreated, infection appears able to continue indefinitely

there’s the same range of symptoms as with disseminated lyme and it can be treated with antibiotic treatment

however, if the disease is treated too late in course, symptoms may remain indefinitely even if bacteria are eradicated because not all damaged host tissues repair quickly/completely so extended antibiotic treatments won’t fix this damage

a minor subset may develop an autoimmnune disease

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29
Q

what happens when lyme disease develops into an autoimmune disease?

A

this is limited to certain MHC haplotypes

MHC presents certain Borrelia antigens in way that resembles certain host tissue proteins

have dual reactive T cells that cause self-reactive immunity

this disease cannot be cured by antibiotics….

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30
Q

how does B. burgdorferi mediate host inflammation?

A

B. burgdorferi lacks LPS or lipoteicoic acid in outer membrane

but B. burgdorferi can make at least 150 different lipoproteins

all lipoproteins possess the same lipid modification = stimulatory

different lipoproteins are expressed by B. burgdorferi in different host environments

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31
Q

what type of genome does borrelia burgdorferi have?

A

segmented genome

linear chromosome of 910 kb

contains 21 plasmids with another 610 Kb pairs –> 12 linear and 9 circular plasmids

over 90% of these genes are unique to B. burgdorferi; many of these genes are lipoproteins

they’re believed to be involved in cycling between host species

but they lack genes to produce biosynthetic enzymes = obligate parasites

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32
Q

what are the virulence factors of B. burgdorferi?

A
  1. outer membrane lipoproteins
  2. endoflagella
  3. inhibits alternate pathway of complement activation
  4. does not require metabolic iron
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33
Q

how does the outer membrane lipoproteins act as virulence factors for B. burgdorferi?

A

the lipoproteins are triacylated and can vary expression on surface of bacteria = immune evasion

there’s a huge repertoire of antigenically distinct lipoproteins

they can restrict access of antibodies to integral membrane proteins

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34
Q

what is the function of endoflagella?

A

B. burgdorferi virulence factor

spirochetal motility

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35
Q

how does B. burgdorferi ihibit the alternate pathway of complement?

A

Erp protein family binds host Factor H

36
Q

what is the benefit of B. burgdorferi not requiring metabolic iron?

A

since it doesn’t need metabolic iron, there’s no competition with host for free iron!

also, it may be insensitive to oxidative host defenses

37
Q

what’s the case definition of Lyme disease?

A

Erythema migrans, observed by a physician. This skin lesion expands slowly over a period of days or weeks to form a large, round lesion, often with central clearing. For surveillance purposes, a solitary lesion must reach a size of ≥5 cm

OR at least one subsequent manifestation AND laboratory evidence of infection

  1. nervous system
  2. cardiovascular system
  3. musculoskeletal system
  4. laboratory evidence
38
Q

what are some of the nervous system effects of Lyme disease?

A
  1. Lymphocytic meningitis
  2. cranial neuritis (facial palsy)
  3. radiculoneuropathy,
  4. rarely, encephalomyelitis.

for encephalomyelitis to be counted for surveillance purposes, there must be evidence in cerebrospinal fluid of the intrathecal production of antibody against B. burgdorferi

39
Q

what are the cardiovascular system effects of Lyme disease?

A

acute-onset, high-grade (2nd- or 3rd-degree) atrioventricular conduction defects that resolve in days or weeks and are sometimes associated with myocarditis

40
Q

what are the musculoskeletal system effects of Lyme disease?

A

recurrent , brief attacks (lasting weeks to months) of objectively confirmed joint swelling in one or a few joints, sometimes followed by chronic arthritis in one or a few joints

41
Q

what lab evidence indicates Lyme disease?

A

1) Isolation of B. burgdorferi from tissue or body fluid,
2) detection of diagnostic labels of antibody against the spirochete by the two-test approach of ELISA and Western blotting (interpreted according to the criteria of the CDC), or
3) single-tier IgG immunoblot seropositivity interpreted using established criteria

42
Q

what would qualify as a confirmed Lyme disease case?

A
  1. a case of EM with a known exposure (as defined above)
  2. a case of EM with laboratory evidence of infection (as defined above) and without a known exposure
  3. a case with at least one late manifestation that has laboratory evidence of infection
43
Q

what would qualify as a probable lyme disease case?

A

any other case of physician-diagnosed Lyme disease that has laboratory evidence of infection (as defined above)

44
Q

what would qualify as a suspected lyme disease case?

A
  1. a case of EM where there is no known exposure (as defined above) and no laboratory evidence of infection (as defined above)
  2. a case with laboratory evidence of infection but no clinical information available (e.g. a laboratory report)

lyme disease reports will not be considered cases if the medical provider specifically states this is not a case of Lyme disease, or the only symptom listed is “tick bite” or “insect bite.”

45
Q

how do you initially screen for Lyme disease?

A

ELISA

crude B. burgdorferi extracts are bound to the well then patient serum containing B. burgdorferi-specific Ab is added

then enzyme-tagged anti-human Ab is added and developed

46
Q

what’s the problem with ELISA-based diagnosis?

A

ELISA uses crude bacterial extracts and many bacteria contain molecules similar to B. burgdorferi like the flagella of other spirochetes or heat shock proteins

so you may get false-positive results due to cross reactivity

you also might get false-negative if tested before antibody response develops

so even if the ELISA is positive you need to confirm with Western blot

47
Q

what results would mean a positive Western blot for Lyme disease?

A

Considered positive if see specific IgG to at least 5 of the 10 B. burgdorferi-specific antigens

for IgM blot, must react to 2 of 3 B. burgdorferi-specific antigens before considered positive (OspC, BmpA, Fla)

48
Q

how do you test for Lyme disease?

A

two-tiered testing for lyme disease

  1. ELISA or immunofluorescence assay
  2. if there’s symptoms for more than 30 days, do IgM and IgG western blot

if it’s symptoms for less than 30 days, IgG western blot ONLY

49
Q

how do you treat Lyme disease?

A

most cases of Lyme disease can be cured with a few weeks of oral antibiotics

doxycycline, amoxicillin, or cefuroxime axetil

patients treated with antibiotics in the early stages of the infection usually recover rapidly and completely

but patients who are first diagnosed with later stages of the disease may have persistent or recurrent symptoms – these patients may benefit from a second 4-week course of therapy

**longer courses of antibiotic treatment have not been shown to be beneficial and have been linked to serious complications, including death

50
Q

how do you treat lyme disease patients with neurological or cardiac forms of the illness?

A

IV treatment of ceftriaxone or penicillin

51
Q

how do you treat a pregnant person with lyme disease?

A

studies of women infected during pregnancy have found that there are no negative effects on the fetus if the mother receives appropriate antibiotic treatment for her Lyme disease

in general, treatment for pregnant women is similar to that for non-pregnant persons

52
Q

how do you prevent lyme disease?

A
  1. avoid tick habitat
  2. wear protective clothing
  3. survey for ticks daily
  4. consult physician after tick bite
  5. learn the early signs of tick-borne illness
  6. control ticks around your home
  7. manage deer populations and movement
53
Q

FLASHCARD: microbiology, pathology, epidemiology, clinical, diagnosis, treatment of borrelia burgdorferi

A

MICROBIOLOGY: Spirochete, not Gram stain, facultative anaerobe, motile, obligate parasite, fastidious

PATHOLOGY: Deposited in skin and disseminate through tissues to all parts of the host. Disease is caused by host inflammatory responses to persistent bacteria. Severity depends on the host genetics, as different patients will have different disease severity though similar number of bacteria.

EPIDEMIOLOGY: Hosted and transmitted by Ixodes ticks, thus see increase in cases during spring-summer. Only see disease contracted in areas with Ixodes ticks, sufficient blood meals to support the tick population, and susceptible vertebrate hosts (e.g. small rodents and certain birds) to maintain the persistent bacteria long-term until can be transmitted to another feeding tick.

CLINICAL: In human skin, often see expanding erythema migrans (bulls-eye) rash at site of tick-bite. General illness symptoms (no respiratory symptoms) are transient. If not treated with appropriate antibiotics, bacteria will persist and re-emerge at different times post-infections, causing inflammatory-mediated diseases in any of the tissues hosting persistent bacteria. Can include arthritis of large joints, varied neurologic symptoms, heart arrhythmia or blockage, skin lesions, or any of a wide variety of symptoms. If not treated until late in disease, may develop symptoms that do not resolve, even after appropriate courses of antibiotics. Subset may develop autoimmune disease.

DIAGNOSIS: Erythema migrans rash in endemic area is diagnostic. Otherwise, need to observe symptoms related to arthritis/musculoskeletal, cardiac, or neurologic Lyme symptoms, then confirm by 2-tier test of ELISA followed by immunoblot of patient serum against antibody standards.

TREATMENT: Early disease responds to doxycycline or amoxicillin. For late/persistent disease, treat with iv ceftriaxone. Extended antibiotic courses are not effective & often have detrimental outcomes

54
Q

what are the symptoms of relapsing fever?

A

persistent fever and aches

NO vomiting, diarrhea, rash, shortness of breath, drainage/discharge, cough, etc

two previous episodes of severe malaise with fever and sweats – felt normal between these episodes

camping the previous months in central Oregon in the desert region but unaware of any tick/mosquito bites

Blood smear taken during the 3rd febrile episode
and stained with Wright-Giemsa showed spirochetes in blood

55
Q

which bacteria are responsible for endemic relapsing fever?

A
  1. B. hermsii
  2. B. parkerii
  3. B. turicatae
56
Q

what is endemic relapsing fever?

A

ornithodores = soft ticks*

endemic in western USA

replicate in blood, neural tissue (turicatae)

reoccurring fever, malaise, etc

lower fatality rate

Jarisch-Herxheimer Reaction = endotoxins released

57
Q

how do you treat endemic relapsing fever?

A

tetracycline

58
Q

which bacteria causes epidemic relapsing fever?

A

B. recurrentis

59
Q

what is epidemic relapsing fever?

A

human body louse!!! (lice)

endemic in Africa & S. America

replicate in blood

reoccurring fever, malaise, etc

higher fatality rate

Jarisch-Herxheimer Reaction = endotoxins released

60
Q

how do you treat epidemic relapsing fever?

A

tetracyclines

61
Q

what areas of the world is tick born relapsing fever endemic?

A

endemic = regularly found among particular people or in a certain area

TBRF is endemic in the western US, southern British Columbia, plateau regions of Mexico, Central & South America, Mediterranean, Central Asia, & much of Africa

62
Q

in what setting do TBRF cases usually happen?

A

most recent cases and outbreaks have occurred in rustic cabin or vacation home settings with mice

people visit rodent infested cabins & start fires and warm cabin produces CO2 and warmth that attract the ticks that transmit TBRF

TBRF normally occurs in summer months when people are traveling to mountainous areas on vacation

63
Q

what is the cycle that happens during the disease process of TBRF?

A

TBRF = tick borne relapsing fever

bacteria replicate to high numbers in blood –> fever spike for 3-7 days

immune responses clear the spirochetes –> normal temperature for 3-7 days

bacteria change their surface proteins (antigenicity) through genetic recombination –> variable membrane protein (VMP)

recombined bacteria replicate to high numbers –> fever spike for 3-7 days

if untreated, cycles can repeat 3-7 times

64
Q

what are the characteristics of TBRF?

A

recurring febrile episodes that last ~3 days and are separated by afebrile periods of ~7 days duration

each febrile episode ends with a sequence of symptoms known as a “crisis“

during the “chill phase” of the crisis, patients develop very high fever (up to 106) where they may become delirious, agitated, tachycardic and tachypneic – this can last 10-30 minutes

then after the chill phase is the “flush phase” which is characterized by drenching sweats and a rapid decrease in body temperature where patients may become transiently hypotensive

overall, patients who are not treated will experience 1 to 4 episodes of fever before illness resolves

65
Q

what are the symptoms of TBRF?

A
  1. headache
  2. myalagia
  3. chills
  4. nauseua
  5. arthralgia
  6. vomiting
  7. abdominal pain
66
Q

how do you diagnose TBRF?

A

definitive diagnosis of TBRF is based on the observation of Borrelia spirochetes in smears of peripheral blood, bone marrow, or cerebrospinal fluid in a symptomatic person

best visualized by dark field microscopy but can also be detected by Wright-Giemsa or acridine orange-stained preparations

specially, the organisms are best detected in blood obtained while a person is febrile

with subsequent febrile episodes, the number of circulating spirochetes decreases – even during the initial episode spirochetes will only be seen 70% of the time

blood samples obtained before antibiotic treatment can be cultured using BSK medium or by inoculating immature mice – spirochetes are usually evident within 24h if blood drawn during a febrile episode

to confirm the diagnosis of TBRF, Borrelia-specific antibody titers should be increased between acute and convalescent serum samples – convalescent serum Ab levels should be at least two standard deviations above pooled negative controls

67
Q

do spirochetes grow on agar?

A

NO

spirochetes will not grow on traditional liquid or agar media

they are obligate parasites

68
Q

what CBC results will you see during TBRF?

A

Incidental laboratory findings include normal to increased WBC count with a left shift towards immature cells, a mildly increased serum bilirubin level, mild to moderate thrombocytopenia (low platelet count), elevated ESR and slightly prolonged coagulation tests, PT and APTT

69
Q

how do you treat TBRF?

A

Erythromycin, tetracyclines, chloramphenicol, or penicillins for 7 days

for young children and pregnant women, either erythromycin and/or penicillin are recommended for treatment of TBRF

when initiating antibiotic therapy, a patient should be watched closely for a Jarisch-Herxheimer reaction for the first 4 hours after the antibiotic is given

70
Q

FLASHCARD: micriobiology, pathology, epidemiology, clinical, diagnosis and treatment of borrelia-mediated relapsing fever

A

MICROBIOLOGY: B. hermsii, B. parkerii, B. turicatae (tick-borne) B. recurrentis. Spirochete, not Gram stain, facultative anaerobe, motile, obligate parasite, only grow in very special medium.

PATHOLOGY: Deposited in skin and disseminate to bloodstream or brain (rare). Bacteria reach critical level that causes high fever, sweats, headache, and chills in response to bacterial lipoproteins until majority are killed by antibody response. However, subset rearrange VMP protein productively to evade antibody clearance. Survivors eventually grow to critical levels again, causing a “relapsing fever”. This can occur up to 4 times before eventually clearing the infection. Louse-borne infections appear more severe that tick-borne disease.

EPIDEMIOLOGY: Hosted and transmitted by Ornithodoros ticks or louse, so only see cases in areas supporting these host/vectors, as well as small rodents to support tick-borne Borrelia. Most tick cases in spring-summer, but can get indoors during winter from hibernating ticks or lice.

CLINICAL: Reoccurring febrile episodes. Last 3 days before ends with a “crisis” of very high fever followed by sweats. Usually recover for 7 days before see relapse of 3-day fever. May repeat up to 4 times.

DIAGNOSIS: Before antibiotic treatment, can often see spirochetes in blood during fever, but before crisis; use dark-field microscopy or Giemsa stain. Eventually can detect RF-associated antibodies, but only after antibody develop. Usually proceed with treatment based on symptoms and epidemiology.

TREATMENT: Erythromycin, tetracyclines, chloramphenicol, or penicillins have all been shown to be effective. If patients undergo Jarisch-Herxheimer reaction, then provide supportive care

71
Q

what disease does borrelia miyamotoi cause?

A

causes disease that resembles relapsing fever

carried in same Ixodes ticks as Borrelia burgdorferi (not a soft tick)

associated with hepatitis and thrombocytopenia

no rash

may be co-transmitted with other pathogens by Ixodes tick

only current test is PCR for presence of B. miyamotoi

72
Q

how do you treat borrelia miyamotoi infections?

A

doxyclycline

73
Q

how is leptospirosis transmitted?

A

it’s shed in the urine of infected hosts

rodents (rats), raccoons, opossums, cattle, swine, dogs, horses, buffaloes, sheep, goats, hedgehogs, frogs

they thrive in certain hosts, but can survive free-living in moist environments for weeks

transmission occurs through direct or indirect transmission from a mammalian host. Indirect transmission via contact with Leptospira contaminated water or soil, is thought to be responsible for most cases.

74
Q

what are the two most common ways to get leptospirosis infection?

A
  1. drinking or contact with water or soil that has been contaminated by urine or body fluids of infected animals

swimming, rafting, kayaking, etc.

leptospirosis is usually acquired by swimming in urine-contaminated water

ingestion is least common route of infection – can be contracted by ingesting contaminated water, but takes much higher loads of bacteria

  1. exposure to the urine or body fluids of infected animals
75
Q

how do spirochetes get inside your body during leptospirosis?

A

spirochete gains access through skin or mucous membranes

they target tissues include kidneys, liver, and eyes

organisms can cross mucus membranes/eye tissues and easily enters through open wounds

76
Q

what happens during the first phase of leptospirosis?

A
  1. phase 1 = flu like symptoms

anicteric syndrome: “flu-like” illness that is usually self-limiting

after 1-2 week incubation, get fever, chills, myalgia, intense headache

if infection not cleared, can develop secondary disease after asymptomatic

77
Q

what happens during the second phase of leptospirosis?

A

differs depending on affected tissues

aseptic meningitis, severe fatigue, liver damage (jaundice is common symptom, including sclerae of eyes), red eyes, hearing loss, respiratory distress, cardiovascular problems

78
Q

what do more severe leptospirosis cases lead to?

A
  1. Weil’s Disease/Syndrome

severe renal and/or liver dysfunction or failure = high fatality rate

  1. some severe cases can involve the lungs –> severe pulmonary hemorrhagic syndrome

CFR = > 50%

79
Q

how do you diagnose leptospirosis?

A
  1. agglutination – seen only after Abs develop
  2. can only be cultured on highly-enriched liquid or agar medium

they produce slow-growing diffuse colonies that grow under surface

depending on disease phase, you can find bacteria in urine or blood

80
Q

how do you treat leptospirosis?

A
  1. tetracyclines (doxycycline)

2. B-lactams

81
Q

what is the most widespread zoonotic disease in the world?

A

leptospirosis

82
Q

what’s the most common way to get leptospirosis?

A

swimming in pee water

83
Q

what are the clinical symptoms of leptospirosis?

A

fever

headache

chills

muscle aches

vomiting

jaundice

anemia

variable rash

84
Q

which groups are at risk for leptospirosis?

A

workers in rice fields, sugar cane plantations, mines, sewer systems, and slaughterhouses; animal caretakers and veterinarians; and travelers to tropical parts of the world involved in recreational activities in fresh water

recreational exposures can include rafting, kayaking, and swimming in tropical and temperate climates.

85
Q

FLASHCARD: microbiology, pathology, epidemiology, clinical, diagnosis, treatment of leptospiroa interrogans

A

MICROBIOLOGY: Spirochete, not Gram stain, facultative anaerobe, motile, fastidious growth. Can be free-living in wet environments for some time, but prefer host.

PATHOLOGY: The incubation period usually is 7 days. Symptoms are variable and include fever, headache, chills, muscle aches, vomiting, jaundice, anemia, & variable rash. If not treated, patient can develop kidney damage, meningitis, liver failure, & respiratory distress; Weil’s disease is severe.

EPIDEMIOLOGY: Infects a wide range of animals. Acquire by drinking or contact with water or soil that has been contaminated by urine or body fluids of infected animals; also get via exposure to the urine or body fluids of infected animals. One of the most common diseases world-wide, but underreported.

CLINICAL: The incubation period usually is 7 days. Symptoms are variable and include fever, headache, chills, muscle aches, vomiting, jaundice, anemia, & variable rash. If not treated, patient can develop kidney damage, meningitis, liver failure, & respiratory distress; lung infection and kidney/liver dysfunction (Weil’s disease) is the most severe and can be fatal.

DIAGNOSIS: May be able to see spirochetes in urine (most common), sometimes blood. Eventually can use agglutinin test to see specific antibodies in serum, but takes time for antibodies to develop. Can only be cultured on highly-enriched liquid or agar medium, and very slow growing and hard to detect on plates. Usually start treatment based on clinical symptoms and epidemiology.

TREATMENT: Treatable with tetracyclines (Doxycycline) or B-lactams

ID Week 3 (25 decks)

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