Ch 12 Chlamydia, Rickettsia Etc

Front 1

Chlamydia and Rickettsia survive in the host by what mechanism?

Back 1

They are obligate intracellular parasites, and they establish "residence" inside animal cells. These "energy parasites" steal ATP from host via ATP/ADP translocator.

Front 2

What is a key difference between Chlamydia and Rickettsia in terms of energy utilization?

Back 2

Rickettsia can oxidize certain molecules and create ATP (via oxidative phosphorylation). Chlamydia does not appear to have this cytochrome system and no mechanism for ATP production.

Front 3

Can we culture chlamydia and rickettsia?

Back 3

Obligate intracellular existance makes it impossible to culture these organism on a media that is "not alive."

We can inoculate Chlamydia or Rickettsia into living cells (usually chick embryo yolk sac or cell culture).

Front 4

What do chlamydia and rickettsia have in common with viruses?

Back 4

They are small and obligate intracellular organisms that use the host cell for their own reproduction.

Unlike viruses, they have both RNA and DNA, make proteins, and are susceptible to antibiotics.

Front 5

Chlamydia transmission

Back 5

human-to-human

Front 6

Rickettsia vector

Back 6

arthropod

Front 7

Chlamydia properties and how is it unique from other gram-negative bacteria?

Back 7

An extremely tiny, gram (-) organism with inner and outer membranes.

It differs from other gram (-) organisms in that it does not have a peptidoglycan layer and no muramic acid.

Front 8

Chlamydia tropism

Back 8

Fond of columnar epithelial cells that line mucous membranes. This coorelates well with the types of infection that Chlamydia causes: conjunctivitis, cervicitis, and pneumonia.

Front 9

Chlamydia life cycle

Back 9

Chlamydia life cycle is complex, and the bacteria exists int wo forms:

1. Elementary body (EB): Metabolically inert (does not divide), dense, round, small (300nm), infectious particle. The outer membrane has extensive disulfide bond cross-linkages that confer stability for extracellular existence.

2. Initial body (also called reticulate body). Elementary body inside host inhibits phagosome-lysosome fusion, and grows to 1000nm. Its RNA content increases-->binary fission-->initial body formation.

Despite all of this IB formation, it still requires ATP from host.

Front 10

Summarize the chlamydia life cycle

Back 10

(EB) is infectious particle that is endocytosed at columnar epithelium-->in the endosome, the EB inhibits phagosome-lysozome fusion and becomes IB--> IBs multiply and some revert to EB-->EBs are liberated and can infect other cells.

Front 11

Chlamydia species

Back 11

1. Chlamydia trachomatis (eyes, genitals and lungs)

2. Chlamydia psittaci

3. Chlamydia pneumonia (only fect lungs)

Front 12

Treatment for Chlamydia

Back 12

tetracycline (blocks 30S ribosome) or erythromycin

Front 13

Chlamydia trachomatis

Back 13

C.T. primarily infects the eyes and genitals. (Clam girl with clam goggles and bikini).

Cause of trachoma (chronic conjunctivitis)--leading cause of preventable blindness (blindness is caused over 10-15 years)

Front 14

Trachoma treatment

Back 14

The conjunctival infection causes inflammation and scarring Scar "trach-tion" pulls and folds the eye inward so that eyelashes rub against the cornea, causing corneal scarring-->infxns-->blindness.

Simple tx. with topical tetracycline prevents this illness.

Front 15

Inclusion cojunctivitis

Back 15

Babies can contract chlamydia trachomatis during birthing as IC. "Conjunctival inflammation iwth a purulent yellow discharge and eyelid swelling" Erythromycin (cidal) eye drops prophylactically.

Basophilic intracytoplasmic inclusion bodies is diagnostic.

Front 16

Infant pneumonia

Back 16

A baby's passage through a chlamydia-infected birth canal may lead to chlamydial pneumonia between 4-11 weeks of life.

Treat with oral erythromycin.

Front 17

Urethritis

Back 17

Urethritis is usually contracted sexually. Neisseria gonorrhea is most infamous for this, but other causes are nongonococcal urethritis (NGU). NGU is predominantly caused by chlamydia trachomatis and ureaplasma urealyticum.

Front 18

Urethritis not caused by neisseria gonorrhea is called non-gonococcal urethritis. NGU is caused predominantly by what two bacterium?

Back 18

Chlamydia trachomatis and ureaplasma urealyticum.

Front 19

If a patient with urethritis is treated with penicillin, which fails, what might this say about the cause of their disease?

Back 19

Chlamydia may be playing a role either as the sole infectious agent or as a part of a mixed infection (Chlamydia is a gram (-) which is unusual in that it has no peptidoglycan layer).

Front 20

Treatment for urethritis:

Back 20

Coverage for neisseria gonorrhoeae, chlamydia trachomatis, and ureaplasma urealyticum.

1. single dose of intramuscular ceftriaxone (cephalosporin) followed by
2. 7 day course of doxy or 1 oral azithromycin (covers chlamydia trachomatis and ureaplasma urealyticum)

Front 21

Cervicitis and Pelvic Inflammatory Disease (chlamydia)

Back 21

Cervix is a frequent site for chlamydia trachomatis infection.

Neisseria gonorrhea and chlamydia trachatomatis can cause this cervical infection which can spread upwards to involve uterus , fallopian tubes, and ovaries.

Front 22

Chlamydia trachomatis

Back 22

A silent sinister "CLAM" chlamydia trachomatis can cause asymptomatic PID that can lead to infertility

Front 23

Treatment of PID

Back 23

ceftriaxone (binding to the 30S ribosomal subunit) in the mRNA translation complex.
and doxycycline (inhibits translation-- prevents the amino-acyl tRNA from binding to the A site of the ribosome) will vanish PID

Front 24

Reiter's syndrome

Back 24

inflammatory arthritis of large joints attributable to chalmydia trachamotis.

Front 25

Fitz-Hugh-Curtis Syndrome

Back 25

Infection of liver capsule with upper right quadrant pain that can occur with either chalmydial or gonoccocal infection

Front 26

Lymphogranuloma venerum (rare)

Back 26

STD caused by chlamydia trachamotis (serotypes L1, L2, and L3) painless papule on genitals with spontaneous healing. Bacteria migrate to regional nodes which enlarge, become increasingly, and may break/drain pus.

Front 27

Chlamydia psittaci

Back 27

(Psittacosis) infects birds, parrots. Humans get infected via inhalation of feathers/dried out poop.

Vets, pet-shop workers, and butchers are all at risk. The atypical pneumonia that results is called "psittacosis" which occurs 1-3 weeks post-exposure.

Front 28

Atypical pneumonias

Back 28

Viral pneumonia, mycoplasma pneumo, chlamydia pneumoniae--> atypical pneumonias.

Sxs: fever, headache, dry hacking cough. Lung exam normal (crackles upon ausculatatoin).

CXR: patches/streaks vs. dense consolidation

Front 29

Rickettsia organismal features and similarities to Chlamydia

Back 29

Gram-negative, non-motile, "rod-to-cocci-shaped" bacterium. Like chlamydia, it is also the size of large virus and is obligate intracellular (steals ATP)>

Front 30

Rickettsia differs from chlamydia in the following three ways:

Back 30

1. Rickettsia requires an arthropod vector (except for Q fever=ticks)

(Ricky the Riding Rickettsia loves to travel. He rides a tick in Rocky Mountain spotted fever, a louse in epidemic typhus, and a flea in endemic typhus).

2. Rickettsia replicates in cytoplasm freely (chlamydia replicates in endosomes)

3. Rickettsia has a tropism for endothelial cells lining blood vessels (chlamydia clams out in columnar epithelium).

4. They cause different disease--most rickettsia cause rashes, high fevers, and nasty headaches.

Front 31

Weil-Felix reaction

Back 31

Proteus vulgaris strains share common antigens with Rickettsia (OX-2, OX-19, and OX-K). The weil-Felix rx. uses cross-reacting proteus vulgaris antigens to help confirm rickettsia dx.

Patient serum is mixed w/ antigens from proteus vulgaris strains. If patient has rickettsial Abs, then the antibodies will bind to proteus vulgaris antigen (which has been complexed with latexbeads) and fall out of solution (agglutinate)

Front 32

Therapy for all rickettsial diseases consists primarily of:

Back 32

1. doxycycline (a member of the tetracycline antibiotic family which blocks 30S subunit) a

2. chloramphenicol (bacteriostatic) (blocks 50S ribosomal subunit)

Front 33

Causative agent of Rocky Mountain spotted Fever

Back 33

Rickettsia Rickettsii

Front 34

Rickettsia Rickettsii

Back 34

"Ricky is riding a wood tick" causes "Rocky Mountain Spotted Fever"

Front 35

Rocky Mountain Spotted Fever symtpoms

Back 35

1 week following wood tick or dog tick bite, and rickettsia rickettsii inoculation, the patient develops the following sxs:

fever, conjunctival redness, severe headache, rash on wrists, ankles soles/palms that spreads to trunk.

RMSF is more common in SE U.S. tick belt than in Rocky Mountain region (so it really should be called appalachian)--> most cases occur in NC SC, tenneesse, okalahoma etc.

Front 36

Pathology of rocky mountain s. fever

Back 36

As previously mentioned, the organism has a tropism for endothelium of small blood vessels and capillaries causing small hemorrhages and thrombi.

Inflammation and damage to small blood vessels explains conjunctival redness/skin rash. Disease resolves in approx. 3 weeks, it can progress to death w/o antibiotic therapy.

Since the tick transmits the bacteria during 6-10 hr. feeding period, early tick removal is preventative of disease.

Front 37

Rickettsia akari

Back 37

(Rickettsialpox) Mite. Transmitted to humans via mites that live on house mice.

So while Ricky plays the Atri, mitey mouse runs through the house. Mite bite leads to localized, red skin bump (papule) at the site of mite bite.

Bump--> Blister-->fever/headache.

Front 38

tx. of rickettsia akari

Back 38

doxycycline and elimination of nearby rodents, which can serve as a reservoir for rickettsia akari, is important in preventing this disease.

Front 39

Rickettsia Prowazekki

Back 39

(Epidemic Typhus)

Ricky is riding a louse...
* Epidemic-- sudden onset/rapid spread of infxn affects a large proportion of population

Endemic--infectious disease that exists constantly throughout a population.

Rickettsia prowazekki causes epidemic typhus

Front 40

two types of rickettsia that cause typhus

Back 40

rickettsia prowazekki (causes pandemic typhus)

Rickettsia typhi (causes endemic typhus)

Closely linked bacteria. Infection with one incurs resistance to the other.

Front 41

Rickettsia epidemic

Back 41

Rickettsia prowazekii is "prowar." War, overcrowding, poverty, and unsanitary conditions allow lice harboring rickettsia prowazekii to take over.

The lice transmit the bacteria causing epidemic typhus to humans.

Front 42

clinical characteristics of epidemic typhus

Back 42

abrupt onset of fever, headache, following a 2-week incubation period. Small pink macules appear around the fifth day on the upper trunk and quickly cover the entire body.

Unlike rocky mountain spotted fever, the rash spares the palms, soles, and face.

Rickettsia invade endothelial cells of blood vessels, there is an increased risk of blood vessel clotting leading to gangrene of feet or hands.

Front 43

Typhus epidemic control measures

Back 43

Besides treatment with tetracycline and choramphenicol, improved sanitation and eradication of human lice will help control epidemics.

Front 44

Rickettsia Typhi

Back 44

(Endemic or Murine Typhus)

endemic, flea-borne typhus is similar to epidemic typhus, yet it is not as severe and does not occur in epidemics.

This disease is caused by rickettsia typhi, with rodents serving as the primary reservoir (Disease is transmitted to humans via the rat flea--Xenopsylla cheopis).

Front 45

Clinical characteristics of Murine Typhus

Back 45

Following a 10-day incubation period, patients can develop fever, headache, and a flat and sometimes bumpy rash develops--just as with epidemic typhus.

Treat with doxy or chloramphenicol. Control flea and rat populations

Front 46

Rickettsia Tsutsugamushi

Back 46

(Scrub typhus or Tsutsugamushi fever) found in asia and SW pacificl. Spread by the bite of larvae (chiggers) of mites. The mites live on rodents, and the larval chiggers live in the soil.

Front 47

Bartonella (Rochalimaea quintana)

Back 47

Causes trench fever, a louse-borne febrile disease. It is rickettsia-like, but named something else because it is not an obligate intracellular organism.

Quintana reflects 5 day lapses patients experience. Like epidemic typhus (Ricketssia prowazekii) both can cause epidemics during wars due to filth and lice overgrowh.

Filth=Lice= Rickettsia prowazekii (epi. typhus) + Bartonella quintana (trench fever)

Front 48

Bartonella Henselae

Back 48

Cat-scratch disease and bacillary angiomatosis.

Cat-scratch disease follows cat bite. A regional lymph node or nodes will enlarge and the patient may develo plow-grade fever and malaise. Disease resolves within a few months without complications.

Henselae may also cause bacillary angiomatosis (proliferation of small blood vessels in the skin and organs of AIDS patients.)

Front 49

Coxiella Burnettii

Back 49

Unique to the rickettsia because, like gram-positive spore formers (clostridium and bacillus) it has an endospore form. This endospore confers properties to the bacteria that differ from other Rickettsiae:
1. Resistance to heat and drying
2. Extracellular existence (thanks spore!), but it still must grow and divide intracellularly with host ATP
3. Non-arthropod transmission (The organism grows in ticks and cattles, and spore aerosolization can cause disease in humans)
4. Pneumonia: due to spore inhalation--> mild pneumonia similar to mycoplasma pneumonia develops.
rupt fever and sweats 2-3 weeks post infxn. This is the only rickettsial disease that causes pneumonia (coxiella) and which lacks a rash.
Also ab

Carol Burnett (coxiella burnetti) coughs after inhaling spores from the cowhide and dired placental products in the grass.

Front 50

Ehrlichia canis and Caffeensis

Back 50

(Ehrlichiosis and Human Ehrlichiosis)

"ehrLICHia canis" is a disease of dogs since dogs like to LICK(LICH), they get bacteria from ticks who jump dog2dog. Ticks can bite humans transmitting Ehrlichias canis's cousin (Ehrlichia chaffeensis) and causes human disease (Ehrlichiosis) that is similar to Rocky Mountain spotted fever.

Causes high fever and severe headache, but only rash rarely.

Front 51

Spirochetes

Back 51

Tiny gram-negative organisms (that look like corkscrews). Move in a spinning fashion via 6 thin endoflagella (axial filaments) which lie between outer membrane and peptidoglycan layer.

Front 52

Spirochete diagnostic

Back 52

Difficult since they can't be cultured with ordinary media. Despite the fact that they have gram negative membranes, they are too small to be seen suing the light microscope.

Special procedures are required:
1. darkfield microscopy
2. immunofluorescence
3. silver stains
(4. serology)

Front 53

3 genera of spirochetes are:

Back 53

1. Treponema
2. Borrelia
3. Leptospira

Front 54

Treponema pallidum

Back 54

(Caustive agent of Syphilis): The # of new syphilis cases has been increasing.

Black heterosexual men women in urban areas at the highest risk for acquisition.

Treponema pallidum enters the body by penetrating intact mucous membranes or by invading epithelial abrasians.

Contact with a skin ulcer with any type of skin can result in infection-->spirochete dissemination throughout body.

Front 55

Stages of treponema pallidum

Back 55

Primary syphylis-->Secondary syphilis-->latent stage-->tertiary stage:

1o stage: (Painless chancre--ulcer)

2o stage:
1. Rash on palms and soles
2. Condyloma latum
3. CNS, eyes, bones, kidneys and/or joints can be involved

Latent syphilis:
25% may relapse and develop secondary stage symptoms again

Tertiary stage:
1. Gummas of skin and bone
2. Cardiovascular (aortic aneurysm)
3. Neurosyphilis

Front 56

Primary syphilis

Back 56

Painless chancre @ inoculation site (3-6 post contact). Regional/non-tender lymphadenopathy. Chancre is firm, ulcerated lesion with punched out base and rolled edges.

Treponema pallidum sheds continuously from it.

Chancre resoltion w/o scarring occurs and represents false hope, because the infection isn't gone

Front 57

Secondary Syphilis

Back 57

Untreated patients enter bacteremic stage (secondary syphilis) 6wks. post chancre. Of course primary-secondary overlap can also occur.

Bacteria multiply-->systemic spread. Systemic=widespread rash, general lymphadenopthy, and organ involvement.

Rash= small red macular lesions over body, palms/soles/oral mucosa. Skin lesions can become papular (bumpy) and even pustular.

Condyloma latum (painless, wart like lesion) in warm, moist sites like vulva or scrotum, can also occur. EXTREMELY CONTAGIOUS.

Patchy bald spots and loss of eyebrows can occur during second stage secondary to skin infection.
Any organ system (CNS, skin, eyes, kidneys and bones) can be affected).

Over 6 weeks rash and condyloma resolve and enter latency.

Front 58

Latent Syphilis

Back 58

So secondary syphilis is gone but serology is not gone. Asymptomatic 75% of time.

After 4 years, relapses fizzle out (now we're non-infectious, unless mother-to-daughter pregnancy transmission).

1/3 of untreated patients will slowly progress to tertiary syphilis.

Front 59

Tertiary syphilis

Back 59

6-40 years to develop with slow inflammatory damage to organ tissue, small blood vessels, and nerve cells. 3 general categories:

1. gummatous syphilis- (3-10 yrs. following primary infection in 15% of untreated patients). Gummas are localized granulomatous lesions which necrose and fibrose. Skin and bone involvement with painless solitary lesions + sharp borders. Antimicrobial therapy is the cure.

2. cardiovascular syphilis- occurs at least 10yrs after primary infxn in 10% untreated. Aneurysms forms in ascending aorta or aortic arch due to small arteriolar destruction (vasa vasorum) supplying the aorta-->necrosis of media layer of aorta. Aortic valve insufficiency-->coronary occlusion (antimicrobial therapy CANNOT reverse)

3. neurosyphilis (8% untreated) w/ 5 common presentationa (a-->e)

a. asymptomatic-- but + CSF

b. subacute meningitis-- high fever, stiff neck, headache (CSF high lymphocyte, high protein, low glucose, + syphilis test) treponema pallidum and mycobacterium TB can cause subacute meningitis w/ lymphocyte predominance

c. meningovascular syphilis: spirochetes attack blood vessels in brain/meninges (circle of willis)-->cerebrovascular occlusion/infarction of brain nerve tissue/spinal cord, and meninges, causing a spectrum of neurologic impairments

d. tabes dorsalid: posterior column and dorsal roots (disruption of vibratory and proprioceptive sense-->ataxia-->reflex loss/loss of pain+temp sense

e. general paresis : progressive brain nerve cell disease-->mental deterioration + psychiatric sxs. (Argyll-Robertson pupil = midbrain lesion= constructs during accomodation (near vision) but NOT TO LIGHT.

Front 60

Syphilis stages

Back 60

(Remember rule of 6's)
Six-Sexual transmission:
1. 6 axial filaments
2. 6 week incubation
3. 6 weeks for ulcer to heal
4. 6 weeks after the ulcer heals, secondary syphilis develops
5. 6 weeks for secondary syphilis to resolve and 66% of latent stage patients have resolution (no tertiary syphilis)
6. six years to develop tertiary syphilis (at least)

Front 61

Congenital syphilis and treatment

Back 61

Fetus of infected pregnant woman. Treponema pallidum crosses placenta, disseminated throughout infected fetus. High mortality rate and almost all survive will develop congenital syphilis early or late.

Early cong. syphilis= within 2 yrs, like severe adult secondary (widespread rash +condyloma latum). Nasal mucous membranes involved-->runny nose "snuffles". Lymph node, liver, spleen enlarge & bone infection.

Late congenital: similar to adult tertiary except cardiovascular involvement is rare
(late cong neurosyphilis = adult neurosyphilis-->deafness common).

Bone/Teeth often involved-->periosteal inflammation-->palatal cartilage and nasal septum destruction-->saddle nose. Similarily destruction of tibia-->saber shins. Upper incisors widely spaced with notch in each tooth (hutchinson's teeth) molars have too many cusps (mulberry molars).

3. Eye disease (ie corneal inflammation) can occur.

Treponema pallidum does not damage fetus until month 4 post-gestation. Antibiotic the mama prior to this time.

Front 62

Mulberry molars are seen in:

Back 62

late congenital syphilis

Front 63

Saber shins are seen in

Back 63

Late congenital syphilis and it is due to periosteal inflammation.

Front 64

Syphilis diagnostic test

Back 64

Since direct spirochete visualization is effective only during the "active" stages of primary and secondary stages, serologic tests were developed of 2 types:

1) NON-specific (cell damage-->release of lipids cardiolipin/lecithin-->measure host antibodies produced to these to diagnose syphilis. This can be done in CSF to dx. neurosyphilis). Nonspecific because 1% of adults w/o syphilis have these antibodies (ie pregnant patients w/ mono, viral hep, IV drug users, post immunized pts).

2) Specific treponemal tests: assay antibodies against spirochete. Patient serum is crossed with non-pathogenic Treponema (this removes non-specific antigens that were developed in response to non-pathogenic treponema in human flora). The post-cross-reacted serum is then crossed w/ pathogenic treponema pall.-->binding = + result.

Front 65

Interpretation of syphilis serology

Back 65

1. + VDRL/RPR & + FTA-ABS= Active treponemal infxn.

2. + VDRL/RPR & - FTA-ABS = probable false positive

3. - VDRL/RPR & + FTS-ABS = successful rx.

4. - - = syphilis not likely (unless syphilis patients also has AIDS, which impairs CD4 Th cells, which impairs B/plasma cell Ab response) OR infxn so recent that immune response hasn't occured yet.

Front 66

Jarisch-Herxheimer Phenomenon.

Back 66

Immediately after antibiotic therapy, most patients will have brief worsening of sxs due to killed organism pyrogen release.

Sxs: Mild fever, chills, malaise, headache, and muscle aches.

occurs with most spirochetes

Front 67

3 Subspecies of "Treponema Pallidum"

Similarities/Differences to Treponema P.

Back 67

All cause non-venereal disease. Do not cause STD syphilis despite the fact that they're morphologically and genetically = to treponema pallidum. Like TP, these strains involve primary skin papule or ulcer development @ inoculation site (usually not genitals)-->sec. stage of widespread skin lesions-->tertiary stage w/skin&bone gummas.

Differences: tertiary stages of nonveneral treponemes don't invade heart/CNS.

3 subspecies:


1. endemicium (endemic syphilis)- skin ulcers/gummas

2. pertenue (yaws)- skin ulcers/gummas

3. carateum (pinta)- skin discoloration only.

Front 68

Tx. of treponemas

Back 68

ONE INTRAMUSCULAR INJECTION OF LONG-ACTING PENICCILN= CURE

And we better be glad penicillin is the miracle drug for syphilis/treponema p. too.

Front 69

Endemicum

Back 69

Subspecies # 1 of Treponema Pallidum (causes endemic syphilis)-- desert zones of Africa and Middle East. Sharing of eating utensils can lead to this.

(Bejel)

Front 70

Pertenue

Back 70

Subspecies # 2 of Treponema Pallidum (Causes yaws)

Yaws is a disease of moist tropics-->spreads human2human via open ulcer contact. Papule appears-->becomes wart-like-->followed by secondary lesions and years later tertiary gummas in skin and long bones.

The tertiary involvement is like JAWS taking bites out of someone's face

Front 71

Carateum

Back 71

Subspecies of Treponema P. # 3- Causes (PINTA)

"POR FAVOR, NO PINTA MI CABEZA"

Hispanic person w/colored red and blue skin lesions "Por favor, no pinta mi cabeza"

Pinta is purely a skin disease limited to rural Latin America. Direct contact-->papule that expands-->2^o eruption numerous red lesions that turn blue in sun-->w/in 1yr. lesions turn white (depigmentation) como PINTA en la cabeza.

Front 72

Borrelia

Back 72

Corkscrew-shape and larger than treponema. Thus viewing w/ light microscopy and giemsa/wright staining is possible.

Cause of Lyme disease (Borrelia burgdorferi) and relapsing fever (caused by 18 other species of Borrelia)-->all transmitted by insect vectors.

Front 73

Borrelia Burgdorferi

Back 73

(Lyme disease) seen in NE, MidW, and NW U.S.

"Ixodes" tick-->transfer lyme agent "borrelia burgdorferi". Again, 24 hr organismal attachment period allows for infection-prevention given tick removal.

Borrelia burgdoferi reservoir: (white-footed mouse and white-tailed deer) and the tick is the vector-->transfers to humans.

While lyme has many features resembling syphilis, both caused by spirochetes, primary stage=single/painless skin lesion.

The lyme primary lesion is (Lyme erythema chronicum migrans) vs. (syphilitic chancre).

Like syphilis, spirochetes spread throughout body, invade organ systems (especially skin). So both organisms cause chronic problems later.

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3 stages of Lyme disease

Back 74

1. Early localized- 10days post bite (lasts 4 weeks), and only has erythema chronicum migrans +flulike illness + lymphadenopthy


2. Early disseminated- dissemination of burgdorferi spirochetes to 4 systems: skin, cns, heart, joints. The lyme juice keeps spreading, but there's not enough juice to go around, so the new lesions are smaller. Borrelia can invade brain, CNs, motor/sensory nerves-->meningitis, CN palsies (bell's), and peripheral neuropathies. Heart abnormalities (10% patients=AV node black) and more rarely myocarditis LV dysfunction.

3. Late stage- 10% develop chronic arthritis >1yr., 1-2peripheral joints, and many of these pts. have B cell allo-antigen HLA-DR (1+4). Encephalopathy can develop featuring memory impairment, irritability, and somnolence.

Front 75

Dx. and Treatment of Lyme disease

Back 75

Clinical findings is first and foremost and analysis of patient travel.

ECM upon presentation can be biopsies/cultured for Borrelia burgdorferi.

CNS/Blood culture difficult, so anti-Borrelia burgdorferi ABs helpful via ELISA and Western immunoblot.

Front 76

Treatment of Lyme

Back 76

Doxycycline or peniccilin family are most effective currently

The ImuLyme and LYMErix, but they are off the market.

Front 77

Borrelia recurrentis

Back 77

(Relapsing Fever) Transmitted to humans via the body louse (other species by tick). This tick feeds on sleeping campers, especially those w/ rodent infestations.

Following transmission, blood dissemination occurs-->high fever, chills, headache, and myalgia (perhaps rash/meningeal involvement).

There are afebrile periods with relapses, with each relapse become shorter and less severel.

Why relapses? Boris the Borrelia is a master at magic "antigenic variation." Post-Ab production/binding, Borrelia recurrentis sneakily /rapidly changes surface proteins. This dance continues for many weeks.

Front 78

Dianosis of Borrelia recurrentis

Back 78

A wright or giemsa-stained smear of peripheral blood during febrile periods may reveal spirochete between RBCs. Darkfield microscopy also useful.

Front 79

Tx. of choice for Borrelia recurrentis

Back 79

Doxy or erythromycin.

Front 80

Leptospira appearance and metabolism

Back 80

Long, thin aerobic spirochetes wound up in a tight coil, with a hook on one or both ends, giving them an "ice tongs" appearance.

Front 81

Two species of Leptospira

Back 81

1. Leptospira interrogans: causes human disease and divided into 23 subgroups and 240 serovars (sub-groups).

2.

Front 82

Leptospira habitat and innoculation

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Found all over the world in urine of dogs, rats, livestock, and wild animals. They can penetrate skin or mucous membranes when humans comes in contact w/ urine either directly or by swimming in contaminated water (and usually some H2O swallowing occurs).

Front 83

Leptospira clinical disease (Leptospira interrogans)

Back 83

1. Leptospiremic phase- bacteria invade blood/CSF-->abrupt high spiking temp, headache, malaise and severe muscle aches. Clasically, conjunctiva are red, and patient develops photophobia.

2. 1 week later, short afebrile period-->fever and sxs recur. This immune phase correlates with appearance of IgM antibodies. Here patients may develop meningismus (CSF-->reveals elev. WC count).

Front 84

Weil's disease

Back 84

a more serious disease caused by contraction of Leptospira (infectious jaundice-->renal failure, hepatitis w/ jaundice, mental status changes, and multi-organ hemorrhage).

Dx= culture on special media (blood/CSF during first febrile phase). 2nd phase-->culture from urine.

Front 85

Treatment

Back 85

Although it's useful to culture blood and CSF (phase 1) and urine (phase 2), you DO NOT want to wait for these test results. Just go by the hx, sxs and specific organ lab tests.

Tx. with peniccilin or doxycycline.