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Spirochete and spirillum
Long, slender, helically curved, gram-negative bacilli
Axial filaments (axial fibrils/endo flagella) facilitate the motility of the organisms
Motility is by rapid rotation around its long axis, like a drill
Treponema, borrelia, Leptospira
Pathogenic spirochete
6-10
Treponema axial filaments
30-40
Borrelia axial filaments
2
Leptospira axial filaments
1
Treponema insertion disks
2
Borrelia insertion disks
3-5
Leptospira insertion disks
Genus Treponema
tightly coiled with a corkscrew appearance
Genus Leptospira
less tightly coiled with sharp hook-like bends at the end of the cell
Genus Borrelia
much less tightly coiled forms which have the appearance of an extremely long undulating bacillary form
Treponoma pallidum subsp. pallidum
Sexual contact or congenital
Worldwide
Venereal syphilis
Group All ages
Treponoma pallidum subsp. pertenue
Traumatized skin comes in contact with an infected lesion (person-to-person contact)
Humid. Warm climates: Africa, South and Central America, Pacific Islands
Yaws
Skin-papules, nodules, ulcers Primary lesions (mother yaw), disseminated lesions (frambesia)
Children
Treponoma pallidum subsp. endemicum
Mouth-to-mouth by utensils (person-to-person contact)
Arid, warm climates: North Africa, Southeast Asia, Middle East
Endemic (Nonvenereal syphilis)
Skin/mucous membrane patches, papules, macules, ulcers, scars; May progress to disseminated oropharyngeal with generalized lymphadenopathy; May demonstrate a latent stage, and late syphilis destructive to skin, bone, and cartilage
Children or adults; rarely congenital
Treponoma carateum
Traumatized skin comes in contact with an infected lesion (person-to-person contact)
Semiarid, warm climates: Central and South America, Mexico
Pinta
Skin papules, macules, and Hyperkeratotic pigments may lead to disseminated skin lesions and lymphadenopathy; a late stage may result in pigmentary changes in the skin (hyper- or hyperpigmentation)
All ages but primarily children and adolescents
Venereal syphilis
contracted during sexual intercourse
Treponema pallidum subsp. pallidum
When we say “Treponema pallidum” without any subspecies after, we are referring to
Primary Syphilis
First clinical sign of syphilis: hard chancre (a painless ulcer) which develops at the site of inoculation
Extremely infectious because the lesion contains a large number of organisms
Bubo formation – appears 1 week after the appearance of hard chancre
10% of patients may have extragenital lesions – face, lips, tongue, tonsils, breast, fingers
Dissemination of the organism occurs during this primary stage. Once the organism has reached a sufficient number, usually within 2-24 weeks then the clinical manifestation of secondary syphilis becomes apparent
Secondary Syphilis
2 to 10 weeks after primary syphilis
Fever, weight loss, malaise, loss of appetite, sore throat, headache (influenza-like symptoms)
Skin is the organ most commonly – rash on the face, scalp, palms of hands, and soles of the feet
Condylomata lata – white mucous patches around moist areas like the anus and vagina (if the patient has this clinical manifestation it is most likely to be syphilis)
Highly infectious state
This is the time when the patient usually seeks medical attention because in the 1st stage, it is only a painless ulcer
Latent Stage
Disease becomes asymptomatic but not necessarily inactive
If you do not receive treatment, you can continue to have syphilis in your body for years without any signs or symptoms
Tertiary syphilis
Appears 3-25 years after the initial infection in up to 35% of untreated px
Gumma formation (definitive characteristic) – granuloma-like lesions that are soft, painless, and noninfectious and found on the skin or in the bones or visceral organs
Central nervous system disease (neurosyphilis), cardiovascular abnormalities, eye disease
Bulldog
Appearance of a deformed maxilla due to mother not seeking treatment or being tested
Saber shin
Bowing of the tibia
Hutchinson’s triad
Deafness, blindness, notched and peg-shaped teeth
Borrelia recurrentis and Borrelia burgdorferi
Causes borreliosis (relapsing fever)
borreliosis
transmission thru the bite of infected body louse or ticks
Borrelia recurrents
Causes Louse-born or epidemic relapsing fever
Humans are the only reservoir (host)
2-15 days before Sx appear
Symptoms:
Fever
Headache
Myalgia
Petechiae
Diffuse abdominal tenderness
Conjunctival effusion
Borrelia burgdorferi
Causes Lyme disease (tick-borne)
Most common vector-borne disease in North America and Europe and is an emerging problem in northern Asia
Leptospira
spiral-shaped, right-handed helices with hooked ends
Leptospira interrogans
Can infect most mammals, reptiles, amphibians, fish, birds, and invertebrates
Causes Leptospirosis
Contact with infected animals or water contaminated with urine or blood of infected animals
2-20 days before Sx appear
Transmission: Enters the human host through breaks in the skin, mucous membranes, or conjunctivae
Anicteric leptospirosis
The most common clinical infection of leptospira
Self-limiting
High fever and severe headache that lasts 3-7 days
“Anicteric” = not affected by jaundice
Weil’s disease/icteric leptospirosis
The most severe illness of leptospira
Liver, kidney, or vascular dysfunction with lethal pulmonary hemorrhage
Death can occur in up to 10% of cases
“Icteric” = affected by jaundice; refer to the serum of px with jaundice
Spirillum minus
Gram (-) thick, spirillum w/ tapering ends
Normal flora of rat’s URT
Causes rat bite fever (Sodoku = Japanese; So = rat; Doku = poison)
Transmission: Bites / scratches from infected rodents
Remedy: pest extermination or cover food to avoid deadly rodent contamination