Please enable JavaScript.
Coggle requires JavaScript to display documents.
Non-Gram Staining Bacteria (Gram Indeterminate (Coxiella burnetii ("…
Non-Gram Staining Bacteria
Mycobacteria
Acid Fast Stain
Intraceullar
Mycobacterium tuberculosis
Special
Intracellular
Glycolipids
in cell wall make strain virulent - Serpentine Cords due to
Cord Factor
Ghon complex - visible calcifications of lung parenchyma and hilar lymph nodes
Hilar lymphadenopathy
Peripheral caseating granulomatous lesion in middle or lower lung - due to growth on hydrophobic surfaces where it mkesa crsytalline monolayer which is toxic and leads to teh formation of caseating granuloma
Caseating Granulomas surrounded by scar with a necrotic center (Tubercle)
Virulence Factors
Transmitted via respiratory droplets
Able to reproduce in macrophages
Mycolic Acids in cell wall
Glycolipids (Cord Factor)
cause bacteria to clump into a serptine formation and gives the bacteria its virulence
protects bacteria from being destroyed by causing granuloma formation
Increases TNF-alpha and activates macrophages which cannot kill the bacteria
Sulfatides
- allows for intracellular survival by preventing phagolysozome fusion sparing the bacteria from exposure to hydrolyses
Sulfatides accumulate in phagosomes creating incompetent secondary lysosomes unable to fuse
Lab Identifiers
Acid Fast (takes up carbol fuchsin stain) due to high concentration of mycolic acids in cell well
Mycolic Acids are waxy fatty acids trap dye
Lowenstein-Jensen Growth Medium
Obligate Aerobe
Positive PPD caused by Type IV HSR
(+) in active infection
(+) in latent infection
(+) in patients with BCG vaccine
Management
Primary TB
RIPE
Rifampin
mutations in mycobacterial RNA polymerase changing the Rifampin binding site
Isoniazid
mutations in the proteins that produce mycolic acid where isoniazid exerts its effect
3.
Pyrazinamide
Ethambutol
Latent TB Prophylaxis
Rifampin
Isoniazid
Diseases
1st is Primary TB typically at lower or middle lobes of the lung and then there are three possible outcomes
Lesions once healed calcify along with the nearby draining lymph nodes
Not many symptoms other than prolonged fever
Most cases resolve, heal by fibrosis/calcification, become latent
Healed Latent Infection
Systemic Infection (Miliary TB)
bacteremia where TB can seed anywhere in the body
bone, liver, lymphatics
Reactivated Latent Infection
Cough possibly bloody
Night sweats
Cachexia - wasting secondary to TNF-alpha overproduction
Affects upper lobes (primary does lower lobes)
typically due to immunosuppression, often due to down regulation of TNF-alpha release needed to activate macrophages and contain the bacteria
screen patients with PPD before giving Inflixumab - anti-TNF-alpha mAb
can affect Skeletal system (Pott's Disease) - infection of spinal colon - can be at multiple levels
can affect CNS causing cavitary lesions (like lacunar infarct)
Mycobacterium leprae
Special
Intracellular
thrives in cold temperatures
reservoir in Armadillo
Well demarcated hairless plaque
Lepromitis Leporsy is due to poor cell mediated (Th1) response.
Virulence Factors
1 thrive in the cold
Lab Identifiers
Acid-fast bacteria due to mycolic acid which takes in acid-fast stain (carbol fuchsin)
2.
Lepodermal Skin Test-
intradermal injection of bacterial antigens to test for presence of immune reaction (similar to PPD) demonstrates good cell mediated response
Biopsy of Leprosy lesion will show lots of bacteria
Management
Tuberculoid
Dapsone
Rifampin
(taken for 6 months)
Lepromitis
Dapsone
Rifampin
Clofazimine
(taken for 2-5 years)
Diseases
Tuberculoid
Th1 response contains the bacteria in macrophages
Mild symptoms but still presents with decrease in sensation
Well demarcated Hairless Lesion
Lepromitis Leporsy
Th2 (humoral) response required here since cell mediated response is weak (Th1 response isn't adequate)
Symmetric Glove and Stocking Neuropathy
poorly demarcated lesions on extensor surfaces
loss of eye brows/eyelashes
collapse of nose
formation of nodular ear lobes
Mycobacterium avium complex
(M avium and M intracellulare)'
Special
Disease of the immunocompromised
CD4 under 50 / mm
Virulence Factors
Acquired via ingestion or inhalation
Lab Identifiers
Intracellular Acid fast staining bacteria
Blood cultures
Histology will show granuloma formation with
foamy epithelioid cells
and Langerhans mutlinucleated cells
Negative PPD
Management
Patients with CD4 under 50
Prophylaxis with weekly
Azithromycin
Diseases
Clinical Features
Fever
Weight Loss
Diarrhea
Advanced Disease
Anemia and hepatosplenomegaly due to reticuloendothelial involvement
Elevated Alkaline phosphatase
Elevated Lactate Dehydrogenase
Pathogenesis
Ingested or inhaled
Phagocytosed by macrophages
Prevent phagolysosome formation
(here the cell mediated response would kill the bacteria but in HIV patients they cannot do this and lack CD4-mediated cytokine release (inferno gamma) to activate the macrophage allowing it to kill the bacteria.
Divide inside macrophages
Spread through the bloodstream and reticuloendothelial system
Spirochetes
Borrelia
("Robin Hood")
Special
Ixodes scapularis vector
Spiral Shaped
No gram Staining
Wright Stain
Giemsa Stain
Bull's Eye Rash
North Eastern USA
Virulence Factors
Tick Larvae
Vector : Ticks have bacteria larvae and feast on a white footed mouse
Reservoir White footed mouse harbors this and serves as the reservoir for the tick
Adult Tick
Vector : ticks again (they harbor the bacteria in their gut)
Obligatory Host: white tailed dear feasted upon by the adult tick
Lab Identifiers
No gram staining due to thin walls
Can be visualized using light microscopy
Wright Stain
Giema Stain
Spiral Shaped
Management
Doxycycline
Ceftriaxone - used for later presentations of the disease
Diseases
Lyme disease
has 3 Stages:
Fever/Chills +
Erythema Chronica Migrans
(Bull's Eye Rash)
not painful nor itchy
within a month of a tick bite
Heart Block with Myocarditis
and Bilateral Facial Nerve Palsy
bilateral Bell's palsy
Arthritis of Large joints
(esp. knee) and Encepalopathy
migratory arthritis
memory problems
cognitive slowing
lymphocytic meningitis
Leptospirosis
(Surfer)
Special
Red painful eyes with no pus
kidney and liver damage
Endemic in tropics
Spiral Shaped / ? Mark Shaped
Due to animal urine in water
Virulence Factors
Excreted in the urine of animals and transmitted to humans when they swim in the contaminated water
associated with water sports
2.
3.
Lab Identifiers
1.
2.
3.
Management
1.
2.
3.
Diseases
Early:
Early spirocytosis : Fever
Conjunctival suffusion - red painful eyes without pus
Late/Severe: Leptospirosis travels in blood
Weils Disease
renal dysfunction as bacteria replicate in kidneys
Fever, high creatinine, azotemia (ask about water sport activity)
liver damage and jaundice due to replication in liver
Treponema Pallidum
("Spiral galaxies").
Special
Dark field microscopy
Painless
genital chancre during Primary
Gumma
during tertiary
Ascending thoracic aortitis
Jarisch-Herxheimer Reaction
Tabes Dorsalis - damage to posterior column
Neurosyphilis - meningoencephalitis
Maculopapular rash on palms and soles
for untreated syphilis (all over the body as well but include the palms and soles which isn't common)
Virulence Factors
Sexually transmitted
Lab Identifiers
Darkfield microscopy
Screening :
VDRL screening test
tests for immune reaction to cardiolipin-cholesterol-lecithin
RPR - Rapid Plasmin Reagent (many false positives)
Mononucleosis
Rheumatoid Factor
SLE
Leprosy
DRG
Confirmation :
FTA antibody Test
contain antibodies specific to T. pallidum
used to confirm positive screening result
Management
Always use Penicillin
Tetracyclines for Pen Allergy but you should
desensitize them to Penicillin because it works the best
Especially if patient is pregnant as tetracyclines are contraindicated
Diseases
Several stages of presentation
Primary
@ genitals
painless genital chancre due to local invasion of blood vessels leading to destruction of nerves and necrosis producing chancre
Secondary
@ Systemic
maculopapular rash on
palms and soles
weeks to months after infection
condyloma lata - has a flat top and doesn't look like a wart (condyloma accumulata looks more like a wart)
Early Latent
Late Latent (tertiary infection)
Gummas
- soft growths with firm necrotic centers that can occur anywhere
Aortitis
(
ascending thoracic aorta
) which can lead to ascending thoracic aneurysm by destroying the vast vasrom which supplies the wall of the aorta
aorta tree barking
Tabes Dorsalis
-
damage to posterior column
loss of proprioception and vibratory sensation
Argyll Robertson pupils
due to ocular Damage - eyes accommodate but don't react to light
pupils stay dilated "Prostitute's Pupil"
Congenital Syphilis
Saber shins - anterior bowing of tibia
Saddle shaped nose - indented bridge
Hutchinson's teeth - notched incisors
Mulberry molars - several enamel out growths
Congenital Deafness
Jarisch-Herxheimer Reaction
dying spirochetes release a massive amount of LPS causing increase in cytokines leading to fever, chills, and headache within hours of starting treatment
indication that the treatment is working
Gram Indeterminate
Coxiella burnetii
("Curly Q the sheep")
Special
Q fever
No RASH
Hepatitis with Pneumonia (shared presentation with Brucella)
Virulence Factors
Spore like structure that can survive digestive tract and survive in poop
Aerosol transmission often from farm animals
Lab Identifiers
Obligate Intracellular
Management
Typically self limited
Acellular vaccine for veterinarian's
Diseases
No Rash
Q fever
Pneumonia
Headache
Fever
Hepatitis
Hepatitis and pneumonia symptoms with animals in history think : Coxiella or Brucella (undulated fever)
Endocarditis in the immunocompromised
Gardnerella Vaginalis
Special
Gram Variable Rod
Smells like fish
Discharge raises pH of discharge
Clue cells
No vaginal inflammation unlike candida or trichomoniasis
Lab Identifiers
Gram Variable Rod
Discharge pH should be above 4.5 (4.5-6.5)
KOH Whiff Test : add KOH to discharge
4.
Clue Cells
epithelial cells diffusely coated with bacteria
Management
Metronidazole
partners needs to be treated as well
Diseases
Elimination of lactobacilli can lead to an increase in anaerobic flora which creates an environment suitable for Gardnerella
Vaginitis with Thin Grayish-White Discharge and
Chlamydia
Special
Leading cause of blindness
Obligate Intracellular
b/c it cannot create its own ATP
Neonatal conjunctivitis doesn't present immediately
Elementary body is the infectious form
Reticular body is the active/diving form
Giemsa Stain
Virulence Factors
2 Stages to Life Cycle
Elementary Bodies
Reticulo bodies
1st Stage : Elementary Body
cell outside of bacteria
2nd Stage : Reticular body
cells inside the host cell and this is when Chlamydia multiplies through binary fission
Final Stage : Release of newly replicated bacteria out of cell and now they're again in their infectious form
Lab Identifiers
Poor Gram staining
Lack of Muramic Acid - component of peptidoglycan that make up the cell wall
Inclusion bodies - reticular bodies diving in the cell
Giemsa Stain
Nucleic Acid Amplification Test - PCR to diagnose
Management
No Muramic Acids so anything that attacks the cell wall is useless
1st line Tetracycline - Doxycycline
Macrolide - Azithromycin
can treat STI as well as Trachoma
new borns need oral Macrolides
for neonatal conjunctivitis
Co-infection often with Gonorrhea
must treat both!
Ceftriaxone added for Gonorrhea
Doxycycline for Chlamydia
Diseases
Chlamydia Trachomatis
Types A-C
:
Blindness - the number one cause of blindness worldwide
Types D-K
: STI
Watery discharge (gonorrhea has white discharge)
can progress to PID and Fallopian tube scarring
Congenital C. Trachomatis :
neonatal conjunctivitis
that presents more than a week after birth (gonorrhea was immediate) and
neonatal pneumonia
with staccato cough (cough with sudden bursts)
Types L1-L3
: Lympho Granulomavenereal Disease (LGD)
Starts as : painless ulcers (like syphillis)
weeks later : tender lymphadenopathy with draining lymph nodes
Reactive Arthritis
(Reiter's Syndrome) - maladaptive immune response that cross reacts and produce antibodies that attack the body
typically @ SI joint and knee
may also present as :
uveitis, urethritis
(all together = Reiter's Syndrome)
Atypical (walking) Pneumonia
- similar to mycoplasma but its more common in the elderly
can also be transmitted by
Chlamydophilis psittaci
transmitted by bird dropping
Rickettsia
("Tennis Match")
Special
Rash
whole body including hands and feet
Prowazekii: Middle-->Out
starts in middle and moves outwards
spares head, feet, and hands
Rickettsii : Out--> In
rash starts on extremities and moves centrally
Vasculitis
+ Obligate Intracellular
Require CoA enzyme
Require NAD+
Lice spreads R. proawazekii
Virulence Factors
1.
2.
3.
Lab Identifiers
No Gram staining
Coccobacilli
Weil-Felix Test
- agglutination test to see cross reactivity between Rickettsia and Proteus vulgaris
Management
Doxycycline
Diseases
Headache and fever are common
Vasculitis and rash
Rickettsia prowazekii
("Football Players")
Rash that starts in the middle
Military camps or Detainment Camps
Spread by Lice
and scratching allows the bacteria to enter the blood
Epidemic Thypus - (Rickettsia Typhi causes endemic typhus)
myalgia
arthralgia
pneumonia
encephalitis
rickettsia rickettsii
-
Rocky Mountain Spotted Feve
("Rock Climbers")
spread by Dermacentor Tick caused by biting
Rash that presents 2-14 days after bite
Rash begins at extremities and spreads centrally
Headache, severe fever, and muscle aches
Mycoplasma pneuomoniae
Special
No cell wall
Cholesterol in cell membrane
Cold-Agglutinins
Eaton's Agar
Lab Identifiers
Sterols in cell membrane
Cold-Agglutinins - 50-70% of patients
IgM antibodies clump to RBC in the cold (IgM cold snowflakes)
Eaton's Agar to isolate
Management
Nothing with activity at cell wall will work as Mycoplasma have no cell wall
Macrolides - erythromycin
Diseases
Most common in young adults : Especially in close contact
military recruits
college kids
Atypical Pneumonia - "Walking Pneumonia" ok presentation with lots of infiltrate
Patchy Infiltrate
Giemsa Stain
Tremponema pallidum
Chlamydia
Intracellular
Mycobacterium
Rickettsia
Chlamydia
Genital Lesions
Painful
Chancroid - multiple deep ulcers
Haemophilis ducreyi
Genital Herpes - multiple small, grouped ulcers
HSV 1 & 2
Non Painful
Granuloma inguinale - extensive & progressive ulcerative lesions without lymphadenopathy
Klebsiella granulomatis
Syphilis - single indurated well circumscribed ulcer with a clean base
Treponema pallidum
Lymphogranuloma venereum + small & shallow ulcers and painful inguinal lymph nodes
Chlamydia trachomatis type L1-L3