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ID Week 4 > ICL 2.15: Chlamydia > Flashcards

ICL 2.15: Chlamydia Flashcards

1
Q

what is the microbiology of chlamydiaceae?

A

gram (-) with unique lPS but no PG

possess inner and outer membranes

contain both DNA and RNA and prokaryotic ribosomes

they synthesize their own proteins, nucleic acids, and lipids –> obligate intracellular parasites; they’re ATP parasites!!

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2
Q

what are the general characteristics of chalmydiaceae?

A

direct destruction of host cells after replication

pretty nontoxic, highly invasive and causes damage from immune system

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3
Q

what’s the developmental cycle of chlamydiaceae?

A

elementary bodies (EB) = infectious forms that are metabolically inactive

reticulate bodies (RB) = noninfectious forms that are metabolically active

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4
Q

which disease syndromes is chlamydia trachomatis responsible for?

A

trachoma biovariant
1. trachoma

  1. conjunctivitis

urogenital biovariant

1. STDS = urethritis, epididymitis,
prostatitis, proctitis, cervicitis,
endometritis, salpingitis, PID,
ectopic pregnancy, infertility
arthritis, infant conjunctivitis,
and pneumonia

LGV biovariant
1. lymphogranuloma venereum

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5
Q

which disease syndromes is chlamydophila pneumoniae responsible for?

A
  1. Pneumonia
  2. upper respiratory
    disease
  3. cardiovascular disease
  4. arthritis
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6
Q

which disease syndromes is chlamydophila psittaci responsible for?

A
  1. psittacosis
  2. abortion
  3. heart tissue damage
  4. arthritis
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7
Q

what two genera has Chalmydia been split into?

A
  1. chlamydia
    ex. chlamydia trachomatis
  2. chlamydophila
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8
Q

what is the cell wall of chlamydiaceae like?

A

their cell wall resembles the cell wall of Gram (-) bacteria with a relatively high lipid content so the gram stain isn’t useful for identifying this organism

instead use Giemsa stain or immunofluorescence

also the cell wall does NOT contain PG but does have penicillin binding proteins (PBP) – this means that cell wall formation is inhibited by penicillins and related B-lactams

however, B-lactam antibiotics are NOT a suitable treatment for Chlamydial infections

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9
Q

why don’t B lactams work as treatment for Chlamydia?

A

chlamydia is an obligate parasite and beta lactams can’t enter our cells, so that would be completely ineffective

chlamydiae are intracellular and neither penicillins nor cephalosporins penetrate human cells adequately

also chlamydia doesn’t have peptidoglycan and beta lactams stop transpeptidase from cross linking peptidoglycan so no peptidoglycan means beta lactams can’t do anything!!

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10
Q

which disease is often present at the same time as chlamydia?

A

about 45% of the cases of gonorrhea have coexisting chlamydial infections

so the recommended treatment of uncomplicated gonorrhea is the administration of both a cephalosporin for the gonococcus and a tetracycline for the chlamydiae

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11
Q

which chlamydia disease is a major cause of urogenital disease?

A

chlamydia trachomatis

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12
Q

what does untreated chlamydia lead to?

A

if left untreated, infection can ascend the endometrial epithelium to the fallopian tubes

severe reproductive complications:

  1. PID

PID can cause scarring of the fallopian tubes, sterility, infertility, ectopic pregnancy, or chronic pelvic pain

  1. 70% of tubal-factor infertility
  2. 35% of cases of ectopic pregnancy

it can also have adverse outcomes during pregnancy like conjunctivitis or passing the infection to the infant

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13
Q

what part of the US most prevlalent?

A

the south = louisiana, georgia, alabama, etc.

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14
Q

are men or women more likely to have chlamydia?

A

black women

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15
Q

what does the prevalence of chlamydia depend on?

A

prevalence is probably actually declining

the actual prevalence of chlamydia depends on the characteristics of the population studied

young age is the factor that is most strongly associated with infection

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16
Q

what are the risk factors for chlamydia?

A
  1. multiple sexual partners
  2. new sexual partner
  3. unmarried
  4. black race
  5. history of or coexistent sexually transmitted infection
  6. cervical ectopy
  7. inconsistent use of barrier contraceptive methods
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17
Q

what is cervical ectopy?

A

Cervical ectopywhen the columnar cells of the endocervix extend beyond the external os onto the vaginal surface, the cervix has a red velvety appearance

as the endocervical epithelium is thinner than squamous epithelium, the more vascular endocervical stroma is seen in the underlying stroma

this is called an ectopy or often referred to incorrectly as erosion

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18
Q

how is chlamydia transmitted?

A

mainly during vaginal or anal sex

also possible through oral sex

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19
Q

which cells does chlamydia infect?

A

it initially infects the single-cell columnar epithelial layers of the endocervix of women and the urethra for men

then it multiplies and spreads to surrounding tissues which leads to inflammation, redness, oedema and discharge

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20
Q

what are the symptoms of chlamydia?

A
  1. inflammation
  2. redness
  3. edema
  4. discharge
  5. mucopurulent cervicitis
  6. non-gonococcal urethritis

however these conditions are often subclinical

infections may also be asymptomatic with burning during urination or an unusual discharge being the only symptom – this is super dangerous!!

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21
Q

what % of chlamydia infections are asymptomatic?

A

≥75% of infected women

25%-50% of men

infected men are more likely to (at least) experience burning during urination

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22
Q

how does chalmydia trachomatis infect the female genital tract?

A

Chlamydia trachomatis elementary bodies infect the columnar epithelial cells of the cervix, which often causes few or no clinical symptoms

but the bacteria can ascend to infect the endometrium and the fallopian tubes, causing pelvic inflammatory disease, tubal inflammation (also known as salpingitis), scarring and occlusion, which can lead to infertility or ectopic pregnancy

the inflammatory reaction is characterized by an influx of macrophages and neutrophils and the formation of immune inductive sites in the submucosa

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23
Q

when does PID happen during a chlamydia infection?

A

PID is initiated when bacteria migrate from the vagina or cervix into the reproductive organs

many different organisms can cause PID, but most cases are associated with gonorrhea and chlamydia

up to 30-40% of acute PID cases are polymicrobial –> infection by N. gonorrhoeae or C. trachomatis may compromise mucosa or spread to parametrial structures, allowing bowel and/or normal flora to invade tissues

24
Q

how do you treat PID?

A

usually treated with at least two antibiotics that are effective against a wide range of infectious agents

must be effective against C. trachomatis and N. gonorrhoeae, as well as against gram-negative facultative organisms, anaerobes, and streptococci

25
Q

what is Reiter’s syndrome?

A

peripheral arthritis lasting longer than 1 month seen with chlamydia infections

strongest correlation is with C. trachomatis infection and/or seroreactivity

inflammatory arthritis of large joints, inflammation of the eyes –> reactive arthritis = triggered following enteric or urogenital infections

initial symptom is often painful urination or increased urination frequency

also associated with urethritis in men and cervicitis in women

sometimes you’ll see mucocutaneous and penile lesions

a small % of patients will also develop small hard nodules on the soles of their feed or hands

symptoms usually resolve after eradicate the infection, but can become chronic

“can’t see, can’t pee, can’t blimb a tree”

26
Q

what is LGV caused by?

A

LGV is caused by serovars L1, L2, and L3 of C. trachomatis

27
Q

what is LGV?

A

LGV is caused by serovars L1, L2, and L3 of C. trachomatis

it enters through skin breaks or crosses epithelial cells of mucous membranes

primary stage is marked by the formation of a painless herpetiform ulceration at the site of inoculation = often unnoticed

then the organism travels via the lymphatics to multiply within mononuclear phagocytes in regional lymph nodes –> this is characterized by painful inguinal lymphadenitis and associated constitutional symptoms

there’s also a tertiary stage of LGV that can occur years after the initial infection = anogenitorectal syndrome may occur with resultant rectal stricture or elephantiasis of the genitalia

28
Q

where in the world is LGV most common?

A

highly prevalent in Africa, Asia and South America

mostly in homosexual men

29
Q

what is the EB form of chlamydia?

A

EB = elementary body

this is the infectious environmentall stable particle that’s analogous to a spore

the highly disulfide crosslinked protein (EnvB) makes the EB resistant to environmental challenges

glycosaminoglycan is found on the surface and is required for attachment to host cells (C. trachomatis)

elementary bodies bind receptors on cells and are endocytosed

they then reside in a host cell surface-derived membrane vacuole = endosome

then EB then reorganizes to become the reticulate body! (RB)

30
Q

what is the RB form of chlamydia?

A

also known as the Initial Body

not stable outside host cell and is fragile because it lacks extensive cross-linked outer membrane proteins

it’s metabolically active but not infectious

it dives by binary fission –> reticulate bodies forms new EB by binary fission until the entire vacuole is filled by EB forming an inclusion

the developmental cycle takes 24-48 hours

31
Q

what is the developmental lifecycle of C. trachomatis?

A

EBs attach to epithelial cells and are internalized via receptor mediated endocytosis

then the endosome matures into phagosome – however, the intact EB prevents vesicle fusion to lysosome

the EB will convert to RB and the RB will replicate by binary fission to form a mature inclusion that contains like 3000 RB

persistence can occur at this stage

then the RBs convert to EBs (the inclusion contains both!)

after 48-72 hours the EBs are released

32
Q

when should you screen for chlamydia?

A

screening for C. trachomatis is indicated in sexually active women with risk factors for this infection, including:

  1. < 25 years old
  2. inconsistent use of barrier contraceptives
  3. a new sexual partner
  4. more than one sexual partner
  5. cervical ectopy
  6. history of or coexisting STD

annual screening would be recommended if any of these are met

33
Q

how do you detect chlamydia?

A

chlamydiaceae are obligate intracellular parasites so they can’t be grown on any known media source

so instead to detect C. trachomatis you have to isolate it in tissue culture; specifically human epithelial cell lines.

  1. direct immunofluorescence staining (IFA)
  2. ELISA (Ab for both of above assay are against MOMP & LPS)
  3. PCR is best

**appropriate sample collection is critical; you have to get into appropriate epithelial layers to get intracellular organisms

34
Q

how do you treat chlamydia?

A

DOC = tetracycline derivatives

ex. Doxycycline for 7 days or single dose of azithromycin

topical application can be used for trachoma

for STDs, both (all) sexual partners need to be treated to prevent reinfection

antibiotics are only effective against the reticulate bodies! and you must take the entire antibiotics course….noncompliance is a big problem

35
Q

how do you treat LGV?

A

doxycycline twice a day for 21 days

36
Q

what is trachoma?

A

an infectious disease caused by bacterium Chlamydia trachomatis

gradual manifestation of the infection causes a roughening of the inner surface of the eyelids

this roughening can lead to pain in the eyes, breakdown of the outer surface or cornea of the eyes, and eventual blindness

chronic conjunctivitis is what can lead to blindness

caused by eyeshadow……

37
Q

how is trachoma transmitted?

A

highly infectious through personal contact

  1. contact with an infected person’s hands or clothing
  2. carried by flies that have come in contact with discharge from the eyes or nose of an infected person (droplet)
  3. vaginal delivery of child from infected mother

because transmission is through close personal contact, it tends to occur in clusters, often infecting entire families and communities

38
Q

where is trachoma common in the world?

A

africa is the most affected continent

almost half of trachoma burden is concentrated in 5 countries = Ethiopia, India, Nigeria, Sudan, and Guinea

but honestly it’s all over the world

39
Q

who is susceptible to trachoma?

A

children are most susceptible to infection, but initial symptoms not too severe

they’re susceptible because they have a poor protective immune response

women are also three times more likely than men to be blinded by the disease which is bad because they’re usually the caretakers in the house!

it’s also a disease of poverty….was used at Ellis Island to turn people away

40
Q

what is the manifestation of trachoma?

A

initial symptoms aren’t severe

but repeated infections over 15-20 years lead to scarring

it causes the eyelashes to turn inward (trichiasis) and scratch the cornea

this leads slowly and painfully to complete blindness…

clindness from trachoma usually strikes adults in their prime years which hinders their ability to care for themselves and their families

by the end their cornea is literally totally opaque and cloudy….

41
Q

which bacteria causes trachoma?

A

chlamydia trachomatis

42
Q

how is trachoma a disease of poverty?

A

women are three times more likely than men to be blinded by the disease and they are traditionally the caretakers of the home

when a woman can no longer perform vital activities for her household, an older daughter is often removed from school to fulfill her mother’s role losing her opportunity for a formal education

without intervention, trachoma keeps families shackled within a cycle of poverty

43
Q

FLASHCARD: microbiology, pathology, epidemiology, clinical, diagnosis and treatment for chlamydia trachomatis

A

MICROBIOLOGY: Gram – cocci, will not Gram-stain, no peptidoglycan, obligate intracellular parasite. Has two-phase life cycle. Elementary body (EB) is infectious, non-metabolically active stable particle. Reticulate body (RB) not stable outside host cell, but replicate intracellular in vacuole until form EB. Are 3 biovars: Urogenital (venereal infect), LGV (Lymphogranuloma venereum), Trachoma (eye)

PATHOLOGY: EBs attach to epithelial cells and enter endosome. Convert to vacuole, where EBs RBs and replicate to large numbers. Eventually convert to EBs and leave host cells after lysis. EBs introduced via sexual contact or contact (Trachoma). UTI: Preferentially infect columnar epithelial layers (cervix in women, urethra in men) to cause persistent infection. Cause cell death and moderate/light discharge. Women often asymptomatic, men usually symptomatic, particularly when urinating. If untreated, infection in women ascend to damage the fallopian tubes and tissues/organs. LGV: Same as UTI, but migrate to draining lymphatic within macrophages to cause LGV. Trachoma: Infect eye via droplet/contact. Get repeated infection of conjunctiva, leading to scarring & blindness.

EPIDEMIOLOGY: Vast majority of the cases in the US are acquired via sexual contact (include oral & anal). Most common in ages 15-25 for both men & women. Also predisposed to lack of barrier contraception, new or multiple sexual partners, African heritage, & living in the South/Midwest US.

CLINICAL: Women are often subclinical; discharge only apparent during exam. Men develop urethritis that causes painful urination and strangury, along with discharge. Discharge is usually lighter compared to gonorrhea. Untreated women often develop PID, similar to gonorrhea, leading to infertility and/or ectopic pregnancy.

DIAGNOSIS: Cannot culture. Test cervical scrapings or urethral swabs using either fluorescent antibodies (IFA) or via PCR for Chlamydia DNA.

TREATMENT: Doxycycline or azithromycin. If UTI, then add Cefixime to treat potential gonorrhea infect

44
Q

how do you treat trachoma?

A

doxycycline or azithromycin

if UTI, then add Cefixime to treat potential gonorrhea infect

45
Q

how do you diagnose trachoma?

A

cannot culture

instead, test cervical scrapings or urethral swabs using either fluorescent antibodies (IFA) or via PCR for Chlamydia DNA

46
Q

C. psittaci vingette

A

a cough of 3 weeks’ duration

fever, chills, shortness of breath, headache, diarrhea, and increasing confusion

CXR showed interstitial pneumonia; prominent in lower lobe of left lung

family had several parrots in the home that were purchased from a roadside stand near the Texas-Mexico border

lab test revealed complement fixation titer for C. psittaci = 1:128

this is a C. psittaci pneumonia infection that is causing psittacosis!

47
Q

what is psittacosis?

A

an acute infection of lower respiratory tract by Chlamydophila psittaci

48
Q

how do you get psittacosis?

A

it’s contracted by inhaling bird feces, urine, or droplets

so people who are at risk are parakeet owners, poultry workers or many other people because any bird can be a reservoir

49
Q

what are the symptoms of psittacosis?

A

initial infection occurs via respiratory tract

you’ll see symptoms at 1-2 weeks which can be mild or asymptomatic like a non-productive cough, CNS involvement or headache

it can also spread to the liver and spleen and produce focal necrosis

there can also be hematogenous spread to other organs..

50
Q

what are the symptoms of severe psittacosis?

A
  1. chills
  2. high fever
  3. cough
  4. confusion
  5. dyspnea
  6. cyanosis
  7. jaundice
  8. interstitial pneumonitis
51
Q

what bacteria causes TWAR?

A

chlamydophila pneumoniae

52
Q

what is TWAR?

A

chlamydophila pneumoniae infection that produces unique pear-shaped EBs with large periplasmic space

it can cause acute respiratory disease but most cases are asymptomatic

this is what causes walking pneumonia in young adults!

53
Q

how is C. pneumoniae transmitted?

A

respiratory secretions

humans are only known reservoir, so is considered a human pathogen

54
Q

where in the body can C. pneumonia grow?

A
  1. smooth muscle cells
  2. endothelial cells of coronary arteries
  3. macrophages
55
Q

which other diseases is C. pneumoniae possibly linked to?

A
  1. heart disease
  2. strokes
  3. Alzheimers
  4. atherosclerosis

still hotly debated though if it’s actually related to any of these…none of it has actually been proven

56
Q

what is the theoretical mechanims behind how C. pneumoniae would cause atherosclerosis?

A

atherosclerosis = a disease of the arteries characterized by the deposition of plaques of fatty material on their inner walls

infected monocytes adhere and migrate into intima = he innermost coating or membrane of a part or organ, especially of a vein or artery

RB –> EB allow infection of other cells

infected macrophage start LDL uptake and oxidation

infected smooth muscle cells proliferate & secrete cytokines and infected endothelial cells secrete inflammatory mediators

further macrophage activation via cytokines elicit tissue factor and metalloproteinases which leads to plaque destabilation and thrombus formation

all of this causes an MI….

57
Q

how does the chlamydiae family cause damage in the body?

A

cause damage by evoking both a cellular and humoral immune response!

but they are treatable with antibiotics that can permeate the host cell (aka NOT B-lactams)

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