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PBD II > Intracellular and Spiral Bacteria - MVP > Flashcards

Intracellular and Spiral Bacteria - MVP Flashcards

1
Q

What is the Mycoplasmataceae cell wall made of?

Gram positive/ Gram negative?

How do they stain?

A

They do not have cell walls.

They stain gram negative (red) but are not truly gram negative or gram positive

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2
Q

Which Mycoplasmatacae produces urease?

A

Ureaplasma

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3
Q

Describe Mycoplasmatacae in terms of intracellular/extracellular

A

In the environment, it is an extracellular bacteria, but in the human host, it is an intracellular parasite

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4
Q

What is this?

A

erythema multiforme

(associated with Mycoplasma pneumoniae)

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5
Q

What is atypical pneumonia?

A

pneumonia which does not respond to penecillin as normal pneumonias do

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6
Q

When would you suspect an infection by Mycoplasma pneumoniae?

A

1
•Causes atypical “walking” pneumonia, acute tracheobronchitis, and bronchiolitis

2
cold agglutinin (anti-I IgM) production

3

  • Associated with Stevens-Johnson syndrome (skin sloughing)
  • Associated with erythema multiforme
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7
Q

Which bacteria can cause non-gonococcal urethritis, cervicitis and pelvic inflammatory disease? (four)

A

Mycoplasmataceae:
M. genitalium, M. hominis

Ureaplasma urealyticum

and Chlamydia trachomatis

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8
Q

Which drug are 45% of Ureaplasma infections resistant to?

A

tetracyclines

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9
Q

How are M. genitalium, M. hominis and Ureaplasma urealyticum diagnosed?

A

Special cultures are required, so these are often treated empirically.

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10
Q

What are these cells infected with?

A

Chlamydia

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11
Q

Describe Chlamydia:

Gram staining?

Intracellular/extracellular?

Shape?

A

gram negative (true)

intracellular parasite

variable - “coccoid to short rods”

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12
Q

What are the two terms for the stages of Chlamydia’s life cycle?

What do they mean?

A

Infectious elementary bodies
outside the cell - able to attach and are internalized by susceptible host cells

Intracellular reticulate (initial) bodies
inside the cell - replicative form
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13
Q

Why MUST Chlamydia replicate inside a host cell?

A

It can not produce enough ATP to replicate on its own.
(actually, seems that it can’t produce any at all?)

It must use an ATP/ADP translocator to comandeer host ATP

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14
Q

Which type of Chlamydia causes upper and lower respiratory tract infections?

A

C. pneumoniae

(strain TWAR, but probably not important to remember that)

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15
Q

What do serovars A, B, Ba & C of Chlamydia trachomatis cause?

A 
Trachoma conjunctivitis (a severe conjunctivitis)
with inclusion bodies that can lead to clouding of cornea and trichiasis (inward growth of eyelashes that can produce severe scarring and blindness)

(seen primarily in children in Africa and Asia)

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16
Q

What do serovars D-K of Chlamydia trachomatis cause?

A

Nongonococcal urethritis, epididymitis, pharyngitis, cervicitis, salpingitis, endometritis, pelvic inflammatory disease, inclusion conjunctivitis (paratrachoma - similar to, but less severe than, trachoma), and neonatal pneumonia

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17
Q

What do serovars L1, L2, & L3 of Chlamydia trachomatis cause?

A

sexually transmitted lymphogranuloma venereum

Small, painless papule or pustule followed by tender lymphadenitis (buboes).

Origional lesion may or may not be present

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18
Q

How is Chlamydia psittaci transmitted?

What does it cause?

A

Inhaled - transmitted by birds

atypical pneumonia and “associated systemic symptoms”

Psittacosis - In psittacine birds (parrots, lovebirds, & parakeets)
Ornithosis – In non-psittacine birds (domestic fowl, ducks, pigeons, turkeys, and many wild birds)

Some sources will refer to both as Psittacosis

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19
Q

How is Chlamydia diagnosed?

A

Clinical presentation
***Identification of inclusion bodies***
PCR
Tissue Cultures
Serology

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20
Q

How are all Rickettsia species transmitted?

A

arthrapod (insect) vector

Bacteria then enter endothelial cells via “induced phagocytosis”

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21
Q

What are these cells infected with?

A

Rickettsia

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22
Q

How does Rickettsia aquire ATP?

A

It can not produce enough ATP to replicate on its own.
(but it can produce some)

It must use an ATP/ADP translocator to comandeer host ATP

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23
Q

Describe Rickettsia:

Gram staining?

Intracellular/extracellular?

Shape?

A

gram negative

obligate intracellular

“pleomorphic” (variable) coccobacilli

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24
Q

What is the pathogenesis that is common to Rickettsia species?

A

Steals host ATP
Replication causes cell lysis
Produces endotoxin

Initial replication occurs at the site of entry
producing a local lesion
followed by vascular dissemination.
Vasculitis ensues, causing
fever, headache and skin rash (petechial hemorrhage)

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25
Q

How is Rickettsia prowazekii transmitted?

How does it present?

What is another name for it?

A

transmitted

  • human to human via human body louse
  • in U.S. via flying squirrels)

presents with:
Fever, horrendous headaches with photophobia, hemorrhagic rash that spares palms & face

called:
“epidemic typhus”

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26
Q

How is Rickettsia akari transmitted?

How does it present?

Also known as?

A

transmitted from mice via mites

presents with vesicular (as opposed to hemorrhagic) rash

AKA: rickettsial pox

**this is the lowest yeild of the Rickettsia species**

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27
Q

What is another name for Rickettsia typhi?

How is it transmitted?

How does it present?

A

endemic/murine typhus

spread from rats via rat flea

Fever, headache, etc., plus centrifugal maculopapular rash

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28
Q

What is another name for Rickettsia rickettsii?

How is it transmitted?

How does it present?

A

Rocky Mountain spotted fever
(actually more common in southeast-southcentral USA)

spread from other mammals via ticks

Fever, etc. plus centripetal (extremities first) maculopapular rash

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29
Q

What is the Weil-Felix test useful for?

Why is it unusual?

How is it done?

A

Used with clinical presentation to diagnose Rickettsia infections

The test uses Proteus vulgaris antigens.
These antigens also happen to react with Rickettsia antibodies.

Patient’s serum is mixed with Proteus vulgaris antigens.
If a reaction is observed, the test is positive.

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30
Q

Orientia tsutsugamushi

Intracellular or extracellular?

Transmitted by?

Endemic where?

Causes what disease?

A

Obligate intracellular parasite
(is not a rickettsia… but in family rickettsiaceae)

Transmitted by chigger (larval trombiculid mites)

Eastern Asia
Southwestern Pacific (Korea to Australia)
and from Japan to India and Pakistan

Causes “Scrub (bush) typhus”
(he spent literally no time explaining this, so the presentation is probably low yeild, but it is listed below)

•High fever, headache, muscle pain, cough, and gastrointestinal symptoms, small painless enlarging papule followed by eschar formation, morbilliform rash, splenomegaly and lymphadenopathy. Pneumonitis, encephalitis, DIC and myocarditis occur in the late phase of illness.

31
Q

Coxiella burnetii

intracellular or extracellular?
gram positive or negative?
requires host ATP?
replicates where?
transmitted how?
causes what disease?

A

Obligate intracellular parasite

Gram negative
(Not a Rickettsia - apparently, CMMRS says otherwise)

Requires host ATP

Replicates only in the phagolysosome

Coxiella burnetii is very highly infectious, and has an “endospore-like state” which is easily aerosolized when in dried animal excretions.

Can also spread via:
unpasteurized milk products
ticks
pets
human to human

Causes:
HIGH YIELD
-Q fever
(asymptomatic, flu-like syndrome or atypical pneumonia)
-Can lead to an immune granulomatous hepatitis

LOW YIELD
-Endocarditis (chronic infection in previously abnormal valves)

32
Q

What is this cell infected with?

A

Ehrlichia

(seen inside the cell like this —> called morulae. Used in Dx)

33
Q

Ehrlichia

Intracellular or extracellular?
Replicates where?
Transmitted how?
Presents with?

A

•Obligate intracellular parasite
(Not a Rickettsia)

Replicates in cell cytoplasm

Tick-borne zoonosis from mammals (including humans)

Infections usually cause fevers, headaches, muscle pain, nausea and vomiting, and fatigue. May have a rash.

34
Q

Which genus does Anaplasma phagocytophilum share most of characteristics with?

What disease does it cause?

A

Ehrlichia

Causes human granulocytic anaplasmosis
(p.k.a. human granulocytic ehrlichiosis)

35
Q

Ehrlichia chaffeensis causes what disease?

A

human monocytic ehrlichiosis

36
Q

How can you tell that this is not a malignancy?

What is it?

A

Bacteria are seen with silver stain

Bartonella infection causing “bacillary angiomatosis”
(Bartonella stimulates proliferation of endothelial cells and blood vessels, causing the tumor)

37
Q

Bartonella

Intracellular or extracellular?
gram staining?
shape?
oxidase present?
seen in what population?
Which cells are the reservoir?

A

Intracellular, non-obligate - “facultative parasite”
(not a rickettsia)

gram negative

pleomorphic bacilli

oxidase negative

immunocompromised patients

erythrocytes

38
Q

Bartonella henselae

Spread how?
Causes which diseases?
Diagnosed via?

A

Cat scratch or cat flees

Cat-scratch disease
(necrotizing lymphadenitis)
bacillary peliosis of liver and bacillary angiomatosis
(typically in immunocompromised patients)

Best - biopsy + silver stain
Can use cultures, but is hard to do.

39
Q

Bartonella quintana

Spread how?
Causes what disease?
Dx via?

A

transmitted from human to human via the body louse

causes trench fever

serology

40
Q

Which bacteria do we see here?

A

Treponema pallidum

41
Q

Treponema pallidum

Intracellular or extracellular?
shape?
gram staining?
other staining?

A

extracellular

heavily coiled (spirochere)

weakly gram negative - blends in with background

use Silver stain to visualize

42
Q

Treponema pallidum

Dx via….

serology?

microscopy?

cultures?

A

clinical presentation

anti-cardiolipin serology [rapid plasma reagin (RPR) or Venereal Disease Research Laboratory (VDRL) tests]

direct treponemal antibody tests [fluorescent treponemal antibody absorption (FTA-ABS)

T. pallidum particle agglutination assay (TPPA) tests]

Darkfield or fluorescent antibody examination of material from lesion

T. pallidum cannot be cultured.

43
Q

Treponema pallidum

describe primary, secondary, tertiary stages
(generally, not for a specific sub-species)

A

Primary
multiplication of the bacteria at the site of entry

Secondary
dissemination of the bacteria after an asymptomatic period, often producing additional symptoms

Tertiary
MAY occur after asymptomatic years to decades.
Often involves gummas, CNS, or CV problems

44
Q

Treponema pallidum pertenue

causes which disease?

transmitted via?

A

“Yaws”

NOT sexually transmitted.
Transmitted by skin-to-skin contact

45
Q

Yaws

  • describe primary, secondary, and tertiary stages
  • endemic where?
A

Painless papule (primary stage)

dissemination after 1-12 months with many papules on face and moist body areas (secondary stage)

followed by gummas (tertiary stage)

endemic:
tropical Africa
S. America
India
Indonesia
Pacific Isles

46
Q

Treponema pallidum carateum

causes which disease?

transmitted via?

A

“Pinta”

NOT sexually transmitted.
Transmitted via skin-to-skin contact.

47
Q

Pinta

  • describe primary, secondary, and tertiary stages
  • endemic where?
A

This is the least severe Trepomonal infection, as its effects are limited to the skin

Painless papule (primary)

followed in 2-18 months by numerous papules on the hands, feet and scalp (secondary)

followed by either depigmentation or hyperpigmentation of involved skin (tertiary)

tropical Central America
South America

48
Q

Treponema pallidum endemicum

causes which disease?

transmitted via?

A

Bejel

Transmission via kissing or by contact with contaminated drinking vessels and pipes
(Gomez said it is from food supply, the internet disagrees)

49
Q

Bejel (endemic syphilis)

  • describe primary, secondary, and tertiary stages
  • endemic where?
A

primary lesion
an oral ulcer

secondary
oral, skin and skeletal lesions

tertiary
gummas with bone and nasal cartilage deformities

occurs in Middle East and Sahara Desert

50
Q

This isn’t a card.

Gomez has been refering to gummas as enlarged lymph nodes involving T palladum infections… but CMMRS and the internet disagree. They define gummas as rubbery granulomas with centers that necrose and become fibrotic.

A

I told you this wasn’t a card.

What are you doing here?

Onward!

51
Q

Treponema pallidum pallidum

causes which diseases?

transmitted via?

A
  • Syphilis – sexually transmitted
  • Congenital Syphilis – in utero OR during delivery
52
Q

This is not a card.

Treponematosis…

According to Gomez, this is a non-sexually transmitted version of T. pallidum pallidum, manifesting similarly to yaws and pinta.

According to the interwebs, Treponematosis simply refers to the group of diseases caused by treponema species, including syphilis, yars, pinta, etc. There does not appear to be a non-sexually transmitted version of T pallidum pallidum, unless you count “congenital”… which is not what he was getting at.

A

Nothing to see here…

53
Q

Syphilis

-describe primary, secondary, and tertiary stages

A

Primary
10- 90 day incubation followed by painless highly contagious hard chancre, generally found on the genitals

Secondary
2-24 weeks later develop disseminated disease with skin rash lasts 2-6 weeks and goes from palms and soles towards trunk and 1/3 will develop infectious condyloma lata.
Approximately 25% of patients experience relapses of the secondary stage

Tertiary
Years later, can develop gumma anywhere in the body.
Cardiovascular syphilis and neurosyphilis are the most frequent causes of death

54
Q

Congenital Syphilis

What are the two forms called?

Describe them.

A
  • Infantile form - symptoms present in first 2 years of life and are variable based on organs infected during dissemination (rash, condyloma latum, desquamation of palms and soles, saddle nose, saber shin)
  • Tardive form – symptoms appear after 2 years of age with Hutchinson triad and other symptoms
55
Q

what is the Hutchinson triad?

A 
interstitial keratitis (eye inflammation)
notched incisors (Hutchinson teeth) 
sensorineural (VIII) hearing loss
56
Q

What is this?

What disease causes it?

Which stage?

A

Condyloma lata

syphilis

secondary

57
Q

Wasserman test

A

•original test used to detect antibodies against cardiolipin
(syphilis Dx)

no longer used.

58
Q

Borrelia

shape?
intracellular or extracellular?
gram positive or negative?
requires host ATP?
transmitted how?
general symptoms?

A

spirochete

extracellular

weakly gram negative

does not require host ATP​

ticks or louse

fever, headache and muscle pain that lasts 4-10 days with relapses

59
Q

Borrelia burgdorferi

disease caused?
(name and describe)

transmission via?

A

Lyme disease

after being bitten by a deer (hard-shell) tick, the patient develops “erythema (chronicum) migrans” - a migrating, bulls-eye shaped erythematous rash.
This may progress to chronic arthritis, with cardiac and neurologic involvement

transmission from rodents via deer ticks (Ixodes scapularis)

60
Q

Borrelia recurrentis

disease caused?
(name and describe)

transmission via?

A

Louse-borne (EPIdemic) relapsing fever

Episodes are more severe but less frequent than ENDemic relapsing fever.

overall, more common than ENDemic relapsing fever, BUT it is LESS common in the USA

spread human to human via lice (Pediculus humanus)

61
Q

Borrelia hermsii

disease caused?
(name and describe)

transmission via?

A

Tick-borne (ENDemic) relapsing fever

overall, less common than EPIdemic relapsing fever, BUT it is MORE common in the USA

spread from rats via soft-shelled tick

62
Q

Leptospira

shape?
intracellular or extracellular?
transmitted how?
causes which disease?

A

spirochete

extracellular

transmitted from rats, mice, moles, and many others via urine
(accidental ingestion or through broken skin or mucosa)

Leptospirosis

63
Q

Leptospirosis

phases?

types?

A
  • Mucosa and broken skin provide entry and get a leptospiremic phase where they localize primarily in the kidneys and shed in the urine (leptospiruric phase)
  • Anicteric leptospirosis - acute onset of headache, fever, rigors, muscle pain, nausea and vomiting, anorexia, diarrhea, cough , pharyngitis, conjunctivitis and/or nonpruritic rash
  • Weil disease (icteric leptospirosis) - described in 1886 is most severe presentation with dysfunction of the kidneys and liver, hepatomegaly, jaundice, and/or alterations in consciousness (hemorrhages)
64
Q

Which bacteria from this lecture are susceptible to macrolide antibiotics?

A

Micoplasma

Orientia tsutsugamushi

Bartonella

65
Q

Which bacteria from this lecture are susceptible to fluoroquinolone antibiotics?

A

mycoplasma

66
Q

Which bacteria from this lecture are susceptible to tetracycline antibiotics?

A

Mycoplasma
(except many Ureaplasma)

Bartonella

67
Q

Which bacteria from this lecture are susceptible to doxycycline antibiotics?

A

Rickettsia

Orientia tsutsugamushi

Coxiella burnetti

Erlichia

Anaplasma

Borrella

Leptospira

68
Q

Which bacteria from this lecture are susceptible to aminoglycocide antibiotics?

A

Bartonella

69
Q

Which bacteria from this lecture are susceptible to Penicillin-G antibiotics?

A

Treponema

Leptospira
(given IV for severe cases)

70
Q

Which bacteria from this lecture are susceptible to amoxicillin antibiotics?

A

Borrella

Leptospira

71
Q

Which bacteria from this lecture are susceptible to ampicillin antibiotics?

A

Leptospira

72
Q

Which bacteria from this lecture are susceptible to cefuroxine antibiotics?

A

Borrella

73
Q

Which antibiotics are Chlamydia species susceptible to?

A

“many common antibiotics”

74
Q
A

PBD II (18 decks)

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