Mycoplasma, Spirochetes, Chlamydia, and Rickettsia II Flashcards
Relapsing fever often described as epidemicor endemic
Borrelia recurrentis
Organism released only after crushing the lice; not transmitted in saliva, excrement or transovarially
Borrelia recurrentis
Transmitted by bites from infected ticks(different than those causing Lyme disease); infected ticks are healthy and transmit transovarially
Endemic relapsing fever (Borrelia recurrentis)
Serve as a reservoir for borella recurrentis
Rodents and small animals
Occurs in certain arthropod vectors as they transmit disease-causing pathogens from parent arthropod to offspring arthropod
Transovarial transmission
Sudden onset of fever with chills, severe headache and malaise lasting 3-6 days and ending abruptly
Relapsing fever
The relapse in relapsing fever occurs
7-10 days later
The severity of symptoms and duration of illness progressively decrease with each
Relapse
Usually associated with a single relapse
Louse-borne relapsing fever
Primarily a disease of wild and domestic animals, human infection through direct or indirect contact with animals
Leptospira
What is the source of infection with leptospira in descending order?
Dogs, livestock, rodents
Chronic renal infection in animals may be asymptomatic leading to continuous shedding of the organism in the urine
Leptospira
Human infection usually indirect, from ingestion of contaminated water or food, or swimming or bathing in contaminated water
Leptospira
Leptospira are viable in water for
Several weeks
Likely very under-reported; may be a prominent zoonosis, especially in tropical regions
Leptospira
Both primary and secondary lesions rich in spirochetes and highly infectious
Treponema pallidium
Most often transmitted by sexual intercourse, but can be transmitted through the placenta or during birth, by kissing, by transfusion of fresh human blood, other sexual contact or by accidental direct inoculation
Treponema pallidum
Can invade virtually any organ in the body and the CNS
Treponema pallidum
Can have active lesions on fingers, breasts, lips, oral cavity or genitals
People infected with syphilis
Heals spontaneously. 30% of infected are completely cured without treatment
Primary stage of syphilus
The secondary stage of syphilis is the disseminated stage where we can see secondary lesions
Anywhere on the body
Serologic tests positive, but no clinical manifestations; 30% stay at this stage if untreated, however blood remains infectious
Latent stage of syphilis
Slow progressing and we can see inflammatory disease affecting any organ in the body
Late (tertiary) stage of syphilis
Symptoms range from subacute meningitis to mental deterioration
Neurosyphilis
Cardiovascular syphilis leads to necrosis of the
Aorta
Lesions in skin (painless) and bone (deep, gnawing pain)
Gummatous syphilis
May result in fetal death and resulting miscarriage, or stillborn at term; signs of congenital syphilis may appear in childhood as developmental abnormalities
Congenital syphilis
What are some of the signs of congenital syphilus?
Notched teeth, saber shins, and saddle nose
Because live bacteria are present in primary and secondary syphilis–ANY physical contact-either sexual, or nonsexual, can
Spread the infection
Can be quickly and directly detected upon examination of exudate from primary, secondary and congenital lesions by dark-field microscopy
T. pallidum
Measure either nonspecific nontreponemal or specific antitreponemal antibodies
Serological tests for T. pallidum
Rely on the fortuitous observation that Ab’s to a lipoidal antigen present in a wide array of host tissues are specifically generated upon syphilis infection
Nontreponemal Tests
These antibodies are referred to as
Reagin
Utilize cardiolipin extracted from mammalian tissue (e.g. beef heart) as the Ag
Nontreponemal Tests
Then addition of lecithin and cholesterol sensitizes the cardiolipin to react with syphilitic reagin, resulting in
Flocculation
What are the two types of tests to measure the presence of reagin?
Flocculation tests and Complement fixation
Reagin in serum can fix complement in the presence of
Cardiolipin
Unfortunately though, generation of reagin antibodies occur in
Other infections
Patients with progressive tertiary syphilis may spontaneously become negative using
Nontreponemal tests
Detect T. pallidum antibodies in patient serum
Specific treponemal tests
Once treponemal Abs are generated, they remain for
A lifetime
What percentage of patients with primary syphilis will be true positives?
60-85%
Which percentage of secondary and tertiary syphilis patients will be truly positive?
100%
What are two examples of common treponemal Ab tests?
- ) FTA-ABS
2. ) TPHA
Indirect immunofluorescence; rabbit T. pallidumas Ag, test for Ab in serum
FTA-ABS (Fluorescent Treponemal Ab)
RBCs treated to adsorb T. pallidum on surface, RBCs then clump when mixed with antitreponemalantibodies
TPHA (T. pallidum hemagglutination)
What are the two major groups of Rickettsia and Orientia?
- ) Spotted fever group
2. ) Typhus group
What are the two components of the spotted fever group?
Rickettsia rickettsii and rickettsia akari
What are the three components of the typhus group?
Rickettsia prowazekii, Rickettsia typhi, and Orientia tsutsugamushi
Severity of diseases these organisms cause is variable depending on the organism and host factors
-All are obligate intracellular organisms
Erlichia, anaplasma, and Coxiella
All organisms except Coxiellaare transmitted to humans by
Arthropod vectors such as fleas, lice, mites, and ticks
A zoonosisin which sheep, goats and cattle constitute the primary reservoirs that shed the organism in urine, feces, birth products and milk
Coxiella Burnetii
Targets columnar epithelial cells that line mucous membranes; correlates well with infections it causes (conjunctivitis, cervicitis, pneumonia)
Chlamydia
Most target endothelial cells that line blood vessels; vascular lesions throughout body produce systemic manifestations and hallmark rash
Rickettsia
The seasonal and geographical distribution of the diseases caused by these organisms is dependent on the habitat of the
Vector
Tick behavior also influences seasonality, clinical presentation and age of human population targeted for tick-borne diseases caused by
Rickettsia rickettsii, Ehrlichia and Anaplasma
In most cases, humans are incidental hosts and do not help propagate the
Organism
The exception to this rule is
-causes louse-borne typhus
Rickettsia prowazekii
Common symptoms of infection in both are fever, headacheand rash
Rickettsia and orientia
Highly adapted for intracellular survival
Rickettsia
Have undergone genomic reduction by relying on their host to provide many essential amino acids, nucleotides and other nutrients; uses transport system to bring these nutrients into the cell
Rickettsia
More closely related to mitochondria than other bacteria
Rickettsia
most virulent of the group, ~5% fatality rate (~25% in the preantibioticera)
Rickettsia rickettsii
Rickettsia rickettsii causes
Rocky mountain spotted fever
Early diagnosis is deceptively difficult because hallmark rash appears 2-4 days after onset of illness
Rocky mountain fever
Rickettsia rickettsii attach to receptors on host vascular endothelial cells via the outer membrane proteins
OmpA or OmpB
Escape from phagosome into host cytosol & proliferate
Rickettsia Rickettsii
Proliferation in cytosol leads to cell damage leading to increased vascular permeability
Rickettsia Rickettsii
Rickettsia rickettsii spread to adjacent cells through hoest cell
Actin-mediated propulsion
A manifestation of the networks of contiguously infected cells
The characteristic petechial rash
Dermacentor variabilis, the American dog tick, is the predominant vector in the eastern two thirds of the United States; Dermacentor andersoni, the Rocky Mountain wood tick, is the prevalent vector in the Western states for
Rocky Mountain Spotted Fever
What is the incubation period for Rocky Mountain Spotted Fever (RMSF)?
2-14 days (median of 7 days)
Disease begins with fever, severe headache, myalgia; rash (90% of patients, petechialin ~50% of cases)
RMSF
Occurs 3-5 days after onset of fever, usually begins around wrist and ankles and spreads toward trunk
Rash from RMSF
Rocky Mountain “spotless” fever (10% of cases) is documented mostly in
Older or black patients
Transmitted to humans through a mouse mite (small and colorless; bite is painless); however seroprevalence high in NYC dogs so another vector suspected
Rickettsialpox
Rickettsialpox is caused by
Rickettsia akari
What are the target cells of Rickettsia akari?
Macrophages/monocytes
Characterized by a primary papule, which ulcerates and forms the dark eschar (clinical hallmark -present 100% of the time)
-At the site of the tickbite
Rickettsialpox
Only Rickettsia that is capable of causing devastating epidemics
Rickettsia prowazekii
Rickettsia prowazekii causes
Louse-borne typhus
Transmitted by close person-to-person contact by the body louse
Louse-borne typhus
The body louse is strictly adapted to humans; it lives in clothes and takes a blood meal
5 times/day
Recently, flying squirrels in the US shown to be stable reservoirs for
R. prowazekii
Now categorized as an agent for bioterrorism (Category B) because it can be aerosol-transmitted and weaponized
R. prowazekii
Severe headache, fever, myalgia and rash that spreads from trunk to extremities (opposite RMSF) is characteristic of
Louse-borne typhus
The louse-borne typhus rash spares the
Face, palms, and soles
The primary illness from R. prowazekii is louse-borne typhus. The recrudescent form is
Brill-Zinsser disease
Thought to arise from stress or from a compromised immune system
Brill-Zinsser disease
Systematic endothelial infection with symptoms similar to RMSF and louse-borne typhis, but usually milder
Murine typhus
Murine typhus is caused by
Rickettsia Typhi
Nearly all cases of murine typhus present with
Fever
Scrub typhus is transmitted transovarally, favoring females. It is caused by
Orientia tsutsugamushi
Unlike most rickettsia, infection does not occur through endothelial cells
Ehrlichia and anaplasma
Infects monocytes and macrophages
Ehrlichia
Infects neutrophils
Anaplasma
Multipy within cytoplasmic membrane-bound vesicles that look like inclusion bodies but are referred to as morula
Ehrlichia and anaplasma
Cell walls are thin because they lack peptidoglycan and LPS
Ehrlichia and anaplasma
Majority of cases in May-August in south-central and southeastern US, i.e. the habitat of the lone star tick, the dog tick, and Ixodes pacificus
Human Monocyte Ehrlichiosis (HME)
Human Monocyte Ehrlichiosis (HME) is caused by
Ehrlichia chaffeensis