Bacteria That Do Not Gram Stain 1

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Chlamydia and Chlamydophila

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do not gram stain
similar to gram-negative :OM, LPS
Obligate intracellular pathogens
energy parasites- use host ATP
Elementary bodies- metabolically inactive, infectious(gamma IFN)
Reticulate bodies- metabolically active, non-infectious

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Chlamydia trachomatis Clinical Manifestation

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Trachoma :Ocular infection, Serotypes A-C
STD (Genital discharge) and perinatal infections
STD (urethritis, cervicitis), pelvic inflammatory disease, neonatal infections
Most common bacterial STD, co-infected with N. gonorrhoeae: Serotypes D-K

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Virulence Factors of Chlamydia

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Intracellular replication
Mechanisms to inhibit MHC Class I expression - decrease antigen presentation to CD8 cells
LPS Inflammation: stimulate TLR-4 to increase IL-1 and IL-8

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Chlamydia Intracellular replication

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Safe from complement, antibodies and phagocytes
Prevents fusion of endosome with lysosomes
Endosome becomes inclusion body for replicating RBs

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Mechanisms for nutrient uptake from cytoplasm into inclusion body containing replicating RBs

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Transporter proteins inserted into membrane of inclusion body
Type III secretion: taking up nutrients from cytoplasm, transport of bacterial molecules into host cell cytoplasm- inhibit apoptosis while RBs divide

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Trachoma

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From Chlamydia
P2P
eye infection
follicular conjunctivitis, lead to chronic inflammation, inverted eye lid, loss of vision
Human pathogen

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Urogenital infections Associated with C. trachomatis

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urethritis or cervicitis -->endometritis(salpingitis) or epididymitis or prostatitis

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Neonatal infections Associated with C. trachomatis

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Ophthalmia neonatorum:Organisms contaminate infant’s eyes in vaginal canal
Pneumonia: if inhaled vaginal fluids

by C. trachomatis and gonorrhea neisseria

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Chlamydophila pneumoniae

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Only one serotype
Respiratory droplets
No animal reservoirs
Mild infections: Sinusitis, Bronchitis, Pneumonia
atherosclerosis -infxn of walls of artery(found in atheromas)

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Spirochetes

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Spiral-shaped bacteria
Gram-negative cell wall structure
IncludesTreponema, Borrelia, Leptospira

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Treponema pallidum

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Spirochete Family
syphilis and congenital syphilis
P2P STD, extracellular organism
Transmitted during primary and secondary.
Primary-painless ulceration on external genitalia, replicates all over body and is asymptomatic
Secondary: Wide-spread rash on trunk, palms, soles. “Great Imitator” -variety of symptoms from different organs
Tertiary: Occurs decades after infection. Diffuse, chronic inflammatory lesions (gummas) in many organs, soft tissue and bone.

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Virulence Factors of Treponema pallidum

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host inflammatory response
Gram-negative cell wall structure, "LPS-like substances"
OM - adherence
fibronectin to avoid phagocytosis
Motility and corkscrew shape andhyaluronidase- aids in spread

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Borrelia burgdorferi

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Spirochete Family
Lyme Disease
Zoonotic infection, no P2P(humans-dead end host)
arthropod borne (ticks) disease
Rodents (mice) serve as reservoir
Erythema migrans- Annular, enlarges

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Life cycle of the Deer Tick

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24 hours before transmission occurs

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Virulence Factors of B. burgdorferi

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flagella - motility

inflammatory lipoproteins in outer membrane (no LPS)

rapidly change surface proteins - for immune evasion

OspA- outer surface protein-adheres to tick epithelial cells

OspC- required for mammalian infection- during blood meal

Coats with mammalian plasmin(clotting protein) to hide

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Pathogenesis of Lyme Disease

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infection through tick bite->erythema migrans-->early disseminated disease--> desseminated disease (migratory arthritis) ---> mo. to yrs later chronic disease: arthritis, neurologic disease

responsive to Ab erythema migrans, early disseminated, and disseminated

not responsive in chronic disease

Attach to, but do not replicate in midgut of tick

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Leptospira

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Spirochete Family

flu-like illness, renal disease

Zoonotic infection
primary reservoir: rodent
incidental hosts: Humans, dogs, farm animals
Shed in urine

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Pathogenesis and Manifestations of Leptospirosis

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Enters skin or mucous membranes

Adhesion structures and LPS are not well characterized

Spreads in body (kidney and liver)

Replicate in small vessels, damage of organs supplied
cross placenta to infect fetus

First phase
abrupt onset of fever, chills, headache, muscle aches, vomiting, or diarrhea, recovery and illness again

Second phase -more severe:
kidney or liver failure or meningitis (Weil's disease)
Antibiotics treatment take several months.