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211 Cards in this Set

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  • Back
What are the major human pathogenic Mycoplasmas, and what are their diseases?
Mycoplasma Pneumoniae - Upper respiratory tract disease, tracheobronchitis

Mycobacteria Hominis - Kidney Infection, pelvic inflammatory disease, postpartum fever.

Mycoplasma Genitalium - Nongonococcal Urethritis

Ureaplasma Urealyticum - Nongonococcal Urethritis
What belongs to the mollicutes class?
What are smaller then some of the larger viruses?
What feature to mycoplasmas lack?
A cell wall.
Mycoplasmas have a coding capacity of about?
700 proteins
What is the carbohydrate profile for:

M. Pneumoniae
M. Genitalium
U. Urealyticum
M. Hominis
M. Pneumoniae - Glucose
M. Genitalium - ???
U. Urealyticum - Urea
M. Hominis - Arginine
The smallest free living bacteria, lack a cell wall, membrane contains sterols, and a slow rate of growth are?
Mycoplasmas and Ureaplasmas
Mycoplasmas and Ureaplasmas are characterized by?
The smallest free living bacteria, lack a cell wall, membrane contains sterols, and a slow rate of growth.
What are the important virulence factors of M. pneumoniae?
P1 - Adhesin. Binds to base of cilia on epithelial cells, leading to their destruction.

Also, the pathogen acts as a superantigen.
Mycoplasma infection and disease occurs in what age groupings?
Most children are infected from 2-5 years of age. Disease most common from 5-15 years of age.

Repeated infections are required before clinical disease is observed
How and when is M. pneumoniae transmitted?
It is transmitted by aerosols, commonly in schools, with no seasonal incidence.
What are the two observed disease forms of M. pneumoniae?
Tracheobronchitis (70-80%) - Bronchial passages primarily become infiltrated withl ymphocytes and plasma cells.

Atypical Pneumonia (a.k.a. Walking Pneumonia, 20-30%) - Patchy bronchitis on radiographs that is more impressive then physical findings.
Atypical Pneumoniae is caused by?
Mycoplasma Pneumoniae
What is the clinical progression and finding in either disease of M. pneumoniae?
Incubation time of 2-3 weeks, with fever, malaise and a ***non-productive cough***.

1 week later, a worsening dry cough with a scratchy sore through. Pleuritic chest pain is rare.

The disease is contagious before and after the end of symptoms.
When is M. pneumoniae contagious?
Before and after symptoms.
What are the 3 immunity pathways to M. pneumoniae disease? What is associated with more severe disease?
Complement activation by Alternative pathway
Production of IgA

Delayed type hypersensitivity reaction is associated with more severe disease
During lab studies, what is the best way to collect a sample for suspected M. pneumoniae? How long does culture take?
Throat washing. Culture takes 2-3 weeks.
What is the cross reactivity of M. pneumoniae?
Cold agglutinin antibodies (IgM) will react with the I antigen of RBC at 4 degrees C.

It can cause cold agglutinin disease, and leukemia.
What is the cold agglutinin test, and what is it good for?
It is effective for Mycoplasma Pneumoniae. It is a non-specific reaction of cold agglutinin antibodies to the membrane glycolipids of Mycoplasma pneumoniae.

It is only effective ~65% of the time.
What is the treatment for M. pneumoniae disease?
Tetracycline and Erythromycin.
M. hominis, M. Genitalium, U. Urealyticum are treated with?
How are M. hominis, M. Genitalium, U. Urealyticum transmitted?
Contamination at birth (especially women) followed by clearance.

In adulthood, they are sexually transmitted.
What are the primary disease manifestations of M. hominis, M. Genitalium, and U. Urealyticum?
Inflammatory disorders of the upper genital tract of women (PID)
What is the revised classification scheme of the Chlamydiaceae family?
Chlamydia - Trachomatis

Chlamydophila - Psittaci, Pneumoniae
Chlamydiaceae are phylogenetically like what bacteria?
Gram Negative
Obligate intracellular parasites requiring host ATP and AA, must be cultivated in cell cultures, biphasic life, resemble Gram negative are?
What is the biphasic life of Chlamydiaceae?
Elementary Bodies (EB) and Reticulate Bodies (RB)

EB - Smaller form, exist extracellularly. Rigid outer-membrane (disulfide bonds), resistant to harsh conditions. Non-replicative, metabolically inactive. Infectious form.

RB - Larger, intracellular form. Frabile outer-membrane (less disulfide bonds). Metabolically active and replicative form. Non-infectious form.
Which form of Chlamydiaceae is the infectious form?
Elementary Bodies
What are the characteristics of elementary bodies?
Smaller form, exist extracellularly. Rigid outer-membrane (disulfide bonds), resistant to harsh conditions. Non-replicative, metabolically inactive. Infectious form.
What are the characteristics of reticulate bodies?
Larger, intracellular form. Fragile outer-membrane (less disulfide bonds). Metabolically active and replicative form. Non-infectious form.
Which form of chlamydiaceae has a rigid outer membrane?
Elementary bodies.
Which form of chlamydiaceae is metabolically active?
Reticulate bodies.
What cells do the infectious forms of chlamydiaceae infect?
The elementary bodies (infectious form) infect columnar, cuboidal or transitional epithelial cells, and sometimes macrophages.
Histologic presence of what is indicative of chlamydiaceae intracellular replication?
An inclusion.
How does a chlamydiaceae infected cell evade cytotoxic cells?
Down regulation of MHC I.
What is the pathogenesis and immunity of chlamydiaceae infection?
The pathogen infects certain types of epithelial cells (columnar, cuboidal, transitional) then to macrophages.

It infiltrates the lymphocytes, leading to lymphoid follicle formation and fibrosis.

Disease results from both destruction of cells and host immune response.

There is no long lasing immunity, leading to chronic and repeated infectious diseases.
What are the diseases and associated serovars of C. Trachomatis?
Serovar A, B, C - Trachoma (leading cause of blindness)

Serovar D ~> K - Inclusion conjuctivitis (newborns), infant pneumonia, cervicitis, nongonococcal urethritis in men

Serovar L1, L2, L3 - Lymphogranuloma Venereum (ocular or urogenital)
What serovars of C. Trachonatis cause Lymphogranuloma Venereum?
L1, L2, L3
What pathogen causes Trachoma?
Chlamydia Trachomatis
What disease does C. psittaci cause?
Chlamydophila Psittaci causes atypical pneumonia
What disease does C. pneumoniae cause?
Chlamydophila Pneumoniae causes atypical pneumonia
What is Trachoma associated with? Where and who is it prevalent in?
Associated with ocular infections.

Often found in areas of poverty and overcrowding (Africa, Middle East, India, SE Asia)

Primarily is a chronic infection in children by repeated contamination by droplets, hands, clothing, flies, and birth canal.
What is the most common STD in the US (and likely world)?
Chlamydia Trachomatis - 50 million new cases worldwide per year.
What is the prevalence in the US of Lymphogranuloma Venereum?
There are approximately 300-500 cases per year, mainly in the male homosexual population.
Where is lymphogranuloma venereum disease most prevelent?
Outside the US - Africa, Asia, South America

In the US - male homosexual population
What is the pathology of Inclusion conjunctivitis?
Serovars D - K

Presents 5-12 days after birth, associated with genital chlamydia.

Mucopurulent discharge from the eye, with corneal infiltrate, vascularization, and scarring. Low probability of blindness.
What is the pathology of Chlamydia Trachomatis infant pneumonia?
Serovars D-K

A wheezing cough and pneumonia without fever. Often begins with conjuctivitis.
What is the clinical presentation of female urogenital infection by C. Trachomatis (D-K)?
80% Asymptomatic

Increased vaginal discharge
Burning during urination
Irritation of area around vagina
Bleeding after sexual intercourse
Lower abdominal pain
Abnormal vaginal bleeding
Risk of premature delivery and ectopic pregnancy

Newborns: Eye symptoms, pneumonia
What is the clinical presentation of male urogenital infection by C. Trachomatis (D-K)?
75% Symptomatic

Clear, white or yellow discharge from urethra
Burning during urination
Itching sensation

**Common cause of postgonococcal urethtritis
What are the 4 methods of diagnosing chlamydial infections with their advantages/disadvantages?
Cytology - Not very sensitive.

Enrichment with cell culture - +iodine stain + antigen detection LPS/OMP

Serology - Hard to distinguish current from past infection (higher IgM)

Nucleic Acid Detection - Kit becoming available, may replace culture
What is the treatment for chlamydial infections?
Tetracycline, Eyrthromycin, Sulfonamides

Safe sexual practice

Treatment of both patients and their sexual partners
How does C. psittaci infection occur?
Chlamydophila psittaci is carried by birds (parrots) and passed to humans through bird droppings.

It is rarely spread through human-human contact.
What is the pathogenesis, diagnosis, and treatment of C. psittaci disease?
Pathogenesis - may have fever, mild influenza-like disease, or, toxic fulminating pneumonitis after incubation of 2-4 weeks. Often spontaneous recovery following 6-8 weeks post-infection.

Diagnosis - serological identification

Treatment - Tetracyclines, Erythromycin
What is the TWAR agents?
Chlamydophila pneumoniae (Taiwan TW-183 USA AR-39)
What is the disease of C. pneumoniae, what is its clinical presentation, and what is its treatment?
Chlamydophila pneumoniae causes atypical pneumonia with person to person spread.

It is mostly asymptomatic or mild in adults.

Severe infection typically involves a single lobe of the lung.

The disease is related to crowded conditions (schools, army dormitory, ect.)

Treatment is Erythromycin or Tetracycline.
What pathogen has been implicated with atherosclerotic lesions?
Chlamydophila pneumoniae
C. pneumoniae has been implicated with what disease process?
Arterial atherosclerotic lesions
What stain is used for Rickettsia?
Giemsa stain, but they are technically gram negative (just with poor staining)
What pathogen is an obligate intracellular organism but has host independent metabolism?
Rickettsia - makes ATP via its own TCA cycle

It also uses membrane transport to jack ATP, AA and metabolites from the host cell
Small gram negative bacteria, but primarily stained with Giemsa. An obligate intracellular pathogen with independent metabolism is?
What are the insect reservoirs for Rickettsia?
Tick, louse, mite, flea.
What are the two strains of Rickettia found in the USA, and what are their diseases?
Rickettsia Rickettsii - Rocky Mountain Spotted Fever

Rickettsia Akari - Rickettsialpox
What are the disease and distributions of:

R. prowazekii
R. typi
O. tsutsugamushi
Rickettsia prowazekii - Epidemic typus (South America and Africa), Recrudescent typus (worldwide), sporadic typhus (USA)

Rickettsia typi - Murine Typhus (Worldwide)

Orientia tsutsugamushi - Scrub Typhus (Asia, Northern Australia, Pacific Islands)
After Rickettsia infects an endothelial cell and escapes the phagolysosome, what are the three methods of extrusion from the cell?
Filipodium focal lysis - R. rickettsii

Budding - O. tsutsugamushi

Lysis of Cell - R. prowazekii
What is the pathogen and vector of Rocky Mountain Spotted fever?
Rickettsia rickettsii. Vector is the hard tick. The tick requires 6-24 hours attachment to spread disease.
What is the defining clinical characteristic of Rocky Mountain Spotted fever?
Rashes on the palms of the hands and soles of the feet (also on arms and legs)
Rashes on the palms of the hands and soles of the feet is associated with what disease?
Rocky Mountain Spotted fever
What causes the complication of RMSF disease?
Destruction of blood vessels leading to gastrointestinal, renal, respiratory and cardiac failure.
What is the mortality of RMSF without treatment?
Up to 20%
What is the prognosis of RMSF without rash?
Poor prognosis
What reaction is used to confirm R. rickettsii infection?
Weil-Felix test (this test is positive for some Proteus strains)
What is the treatment for R. rickettsii (RMSF) infections?

Tetracycline, chloramphenicol
What is the disease, progression, and treatment associated with R. akari?
Rickettsial Pox

Vector - mites
1 week incubation at the bite site. 1-3 weeks later FCHM begin, with a generalized rash at bite site.

Mild disease with rare fatalities.

Treatment is tetracycline of chloramphenicol
What is the disease, vector, progression, detection, and treatment R. prowazekii?
Epidemic Typhus, or the milder form, Brill-Zinsser disease

Vector - louse

Incubation 1 week, followed by FCHM and maculopapular rash from trunk to extremities

Complications - mycarditis, stupor, delirium.

High mortality (60-70%)

Detection - Serology

Treatment is tetracycline or chloramphenicol
What is the disease, vector, progression, detection, and treatment R. typhi?
Endemic typhus

Vector - rat flea

Incubation of 1 week followed by maculopapular rash from trunk to extremities. Mild disease that often resolves by itself

Detection - Serology

Treatment is tetracycline of chloramphenicol
What is the disease, vector, progression, detection, and treatment O. tsutsugamushi?
Scrub typhus

Vector -chiggers

Incubation of 1 week followed by FCHM and maculopapular rash from trunk to upper extremities. Disease is variable but may be severe.

Detection - Serology

Treatment is tetracycline or chloramphenicol
Small, intracellular bacteria. Stain with Giemsa stain, transmission by tick, and causes leukopenia and thrombocytopenia is?
Ehrlichia Chaffeensis
What are the characteristics of Ehrlichia Chaffeensis?
Small, intracellular bacteria. Weakly gram stains, Giemsa stain is the best.
Transmitted by tick.
Infection of leukocytes: leukopenia, thrombocytopenia, elevated serum transaminase
What disease does Ehrlichia Chaffeensis cause in humans?
Human Ehrlichiosis.

Infection of leukocytes causes leukopenia, thrombocytopenia, and elevated serum transaminase.
How does Erlichia Chaffeensis survive and multiply in the host?
Erlichia Chaffeensis is taken up into phagocytic vesicles of leukocytes. The bacteria inhibits fusion of the phgosome and lysosome. The bacteria replicates inside the phagosome.

The bacteria leaves the cell by lysing both the phagosome and cell membrane.
How is disease caused by Erlichia Chaffeensis diagnosed and treated?
Erlichia Chaffeensis disease is diagnosed by serology or DNA probes.

It is treated with doxycycline.
What causes Q fever?
Coxiella Burnetii
Coxiella Burnetii causes what disease?
Q fever
Small, intracellular bacteria. Gram negative (stains poorly), Giemsa stain. Replicates in phagolysosome of macrophages, possesses two transmission cycles is?
Coxiella Burnetii
Coxiella Burnetii is characterized by?
Small, intracellular bacteria. Gram negative (stains poorly), Giemsa stain. Replicates in phagolysosome of macrophages, possesses two transmission cycles.
What are the two transmission cycles of Coxiella?
1) Arthropods transmit Coxiella among sheep, cattle and goats.
2) Infected animals shed organisms in milk, urine, and feces.
-Organism can survive long periods of time in environment
-Human infection follows ingestion of raw milk, inhalation of infectious dust and direct exposure of skin/mucous membranes to infected animal products.
What is the clinical presentation of Q fever?
Fever, chills, headache, myalgias (FCHM).
GI symptoms, sore throat, atypical pneumonia similar to Mycoplasma pneumoniae and Chlaymydia psittaci
Hepatosplenomegaly in ~50% of cases.

Chronic disease leads to endocarditis
Fetal infection reported in women exposed to infected animals/products
How is Q fever diagnosed?
An appropriate patient history with serology.

Cultivation is not recommended - dangerous.
What is the treatment for Q fever?
Tetracycline, chloramphenicol.

Chronic infection may require prolonged therapy.
How is Coxiella infection prevented?

A vaccine is available but not used.
Gram negative rod, aerobic, causes trench fever and catscratch disease is?
Bartonella quintana - Trench fever
Bartonella henselae - Catscratch disease
What causes Trench fever?
Bartonella quintana
What causes Catscratch disease?
Bartonella henselae
Bartonella henselae causes what disease?
Catscratch disease
Bartonella quintana causes what disease?
Trench fever
What is Trench fever, and what causes it?
Caused by Bartonella quintana, the disease presents with FCHM and severe pain in the tibia that recurs on a 5 day cycle (hence the name).

Sometimes it presents with a rash, and disease has a low mortality rate.
What is the transmission vector for Bartonella species?
What is the presentation of Catscratch disease, and what causes it?
Caused by Bartonella henselae.

Disease presents about 2 weeks after contact. Edema and pain in the lymph nodes. Symptoms are mild to severe, and may include malaise, anorexia, or both.
What is the second most common STD in the US?
Neisseria Gonorrheae
Aerobic, gram negative diplococci, oxidase and catalase positive is?
Neisseria Gonorrheae
Neisseria Gonorrheae is characterized by?
Aerobic, gram negative diplococci, oxidase and catalase positive.
What virulence factor of N. gonorrheae displays antigenic variation?
PilE protein, the Pilin protein that is the major fimbrial protein that initially binds to epithelial cells.
What are important virulence factors to N. gonorrheae?
PilE (pilin, antigenic/phase variation), IgA protease, Beta lactamase
What are the symptoms in men and women of N. gonorrheae infection?
Men - purulent discharge from penis with accompanying pain and burning upon urination.

Women - Cervix infection, purulent discharge from the vagina **May be asymptomatic in its early stages**. Leads to PID
How does N. gonorrheae progress in women?
Following initial infection, it can move beyond the cervix, infecting the fallopian tubes and causing pelvic inflammatory disease (PID). This can lead to sterility and/or ectopic pregnancy.
How is N. gonorrheae cultured?
on Thayer Martin agar.
What is the leading cause of purulent arthritis in adults?
Neisseria gonorrheae
What is the presentation of Gonococcemia?
Disseminated infection with septicemia and infection of skin and joints. Occurs in 1-3% of infected women.
What is Waterhouse-Friderichsen syndrome, and what is it a complication of?
Hemorrhagic adrenalitis, it is a complication of Neisseria Meningitidis (meningococcemia)
How can neonates become infected with N. gonorrheae?
During vaginal delivery, if the mother is infected it can spread to the fetus. The organism commonly infects the eye, and can even lead to blindness.
What STD commonly infects the eyes of newborns and can lead to blindness?
Neisseria gonorrheae
What is the treatment for N. gonorrheae?
Ceftriaxone (a beta-lactamase resistant cephalosporin)

Organism commonly possesses beta-lactamase activity.
Why is there no vaccine for N. gonorrheae?
Strains are highly variable in antigenic determinants, particularly pilin (PilE, phase variation) and other out membrane proteins.
What are the three genus's of spirochaetaceae?
Treponema, Borrelia, Leptospira
Gram negative, long, thin, helical and motile are?
What is the causative agent of syphilis?
Treponema pallidum
Treponema pallidum causes what disease?
How is syphilis transmitted?
Genital/Genital contact with a chancre.

Also, transmission can occur in utero or during birth.
How is Treponema pallidum identified in primary syphilis? In secondary and tertiary syphilis?
Primary syphilis - Dark field microscopy or fluorescent antibody staining.

Secondary/Tertiary syphilis - Serological methods to detect Cardiolipin (results from tissue injury with autoimmunity). If positive, more definitive diagnosis is achieved by detection of specific serum antibodies
How is syphilis treated?
Treponema pallidum - syphilis

Treated by penicillin (injection)
Or by tetracycline/doxycycline in penicillin allergic patients (not for neurosyphilis)
What is Bejel? How does the disease progress?
Endemic syphilis.

Skin or mucous membranes are the first to be infected, but the bacterium can spread deeper to the bones. Major malformation of the face and limbs can result.
What are the nonvenereal treponemal diseases?
Bejel, yaws, and pinta
How is Bejel spread? Where is it common?
Non-sexual contact. i.e. hands to broken skin.

It is common in low income groups of poor hygeine. Commonly found in Middle-east, Africa, Australia and central Asia
What are is the clinical presentation and progression of Yaws?
Caused by Treponema pertenue.

Spread by direct contact to skin lesions. After about a month of infection, a papule forms at the infection site which transforms into a crusted ulcer that takes months to heal.

Painful swelling of the lymph nodes occurs. Later, soft growths appear on the face, buttocks and limbs.

The growths can occur on the feet, producing a characteristic walk, gives rise to the name "crab yaws"

Can lead to further formation of tumors and ulcers on the face can cause bone malformation and be severely disfiguring.
What causes Yaws?
Treponema pertenue
What is the treatment of Yaws?
Single penicillin G injection which can be completely curative.
What causes Pinta?
Treponema carateum
Where does Pinta occur?
The 'New World', particularly the Caribbean, Central america and northern South America.
What is the treatment for Pinta?
Single penicillin G injection which can be completely curative.
How is Pinta spread?
Personal contact through cuts in the skin.
How is Pinta detected?
Via serology, or direct examination of lesion specimens under light microscopy.
What disease is caused by B. burgdorferi?
Lyme Disease
What is the vector for Lyme disease?
B. burgdorferi, carried by soft-shelled ticks.
What are the three Borrelia pathogens, and how are they transmitted?
Borrelia recurrentis - Human louse
Borrelia hermsii - Soft-shelled tick (rat population)
Borrelia burgdorferi - Soft-shelled tick
What are the three stages of Lyme disease?
1) Erythema chronicum migrans (days)
2) Arthritis, CNS, cardiac disease (week/month)
3) Chronic disease (month/year)
What diseases do B. recurrentis and B. hermsii cause?
Relapsing fever
What is the characteristic presentation of Lyme disease?
The "bullseye" rash - Erythema chronicum migrans
How is Borrelia infection diagnosed?
Most important is from patient history.

Microscopy, mouse enrichment, culture, and serology are all not very efficient.
How is Lyme disease treated?
Borrelia burgdorferi

Early treatment with doxycycline, amoxicillin, and cefuroxime axetil

In the case of arthritis (late progression), I.V. therapy is preferred to oral or intra-muscular administration.
What disease is caused by L. interrogans? What are is colloquial names?
Causes Leptospirosis.

Also known as:
Weil's disease
Sewerman's flu
Canicola fever
Hemorrhagic jaundice
Mud fever
Swineherd's disease
What causes Weil's disease?
Leptospira interrogans
How is L. interrogans transmitted?
The pathogen infects many animals and is ***Excreted in the urine***.

Contact of skin or mucous membranes with contaminated water, soil, vegetation, or direct contact to urine or tissues of infected animals can spread.

Also by ingestion of contaminated foods, or inhalation of droplet aerosols of contaminated fluids.
What are the clinical signs of L. interrogans infection?
Leptospira interrogans

Fever, headache, chills, severe malaise, vomiting, myalgia and conjunctival suffusion.

Occasionally meningitis, and rash.

Sometimes jaundice, renal insufficiency, anemia and hemorrhage of the skin
How is L. interrogans detected?
Dark field microscopy, immunofluorescence, light microscopy after appropriate staining.
How is Weil's disease treated?
Leptospira interrogans

Penicillin or tetracyclines
How is L. interrogans treated?
Leptospira interrogans

Penicillin or tetracyclines
What is the prophylaxis for L. interrogans?
What is an infection acquired in a hospital or healthcare facility called?
Nosocomial infection
What are the predominant organisms of nosocomial infections?
Gram Negative Bacilli - Pseudomonas aeruginosa, Acinetobacter, Klebsiella
Staph aureus
Coagulase-negative staphylococci

What is the trend in nosocomial microorganisms?
More Gram positive microorganism trend

Fungal infections are increasing
What are most hospital acquired infections spread by?
What are the symptoms associated with meningitis?
Severe Headache
Stiff neck
Dislike of bright lights
Drowsy/Less Responsive
What are the most common causes of bacterial meningitis in children aged 0-4 weeks?
Strep Agalactiae (Group B)
Escherichia coli
Listeria Monocytogenes
Klebsiella pneumoniae
Enterococcus spp.
Salmonella spp.
What are the most common causes of bacterial meningitis in children aged 4-12 weeks?
*S. pneumoniae
*N. meningitidis

S. agalactiae (Group B)
E. coli
L. monocytogenes

~Haemophilus Influenzae
What are the most common causes of bacterial meningitis in children aged 3 months - 18 years??
N. meningitidis
What are the most common causes of bacterial meningitis in children aged 18-50 years?
S. pneumoniae
N. meningitidis
What are the most common causes of bacterial meningitis in children aged over 50 years?
S. pneumoniae
N. meningitidis
L. monocytogenes
aerobic gram negative bacilli
What is the most common cause of meningitis in children and young adults?
N. meningitidis
What deficiency increases risk of neisseria infection?
Terminal Complement Deficiency
What is the most frequently observed agent of bacterial meningitis in the US?
S. pneumoniae
L. monocytogenes meningitis is common in what age groups?
Infants <1 month and adults > 60 years, and all immunocompromised (cancer, alcoholics, steroid therapy recipients, etc.)
What is the most common cause of meningitis in neonates in the US?
Group B Streptococcus
Meningitis caused by Staphylococcus aureus is usually found in what groups?
Early post neurosurgical or post-trauma patients
When is the risk of syphilitic meningitis greatest?
During the first 2 years after infection
What happens to protein and glucose in the CSF in the presence of bacterial meningitis?
Protein increases
Glucose decreases
What can be administered in addition to antibiotics for suspected bacterial meningitis?
What are the 4 major zoonotic diseases?
What are the 4 forms of Brucella disease?
Brucella melitensis - severe, acute disease
Brucella suis - chronic destructive disease
Brucella abortus - mild disease
Brucella canis - mild disease
What is Brucellosis called in animals?
Bang's disease or contagious abortion
What is disease caused by Brucella called in humans?
Brucellosis, Undulant Fever, or Malta Fever
Gram negative, nonmotile, coccobacilli, strict aerobes, grow very slowly on blood agar, and live as facultative intracellular pathogens in the host are?
Brucella is characterized by?
Gram negative
Strict aerobes
Grow very slowly on blood agar
Facultative intracellular pathogens in the host
B. abortus releases 5'-guanosine and adenine, which are capable of what?
Inhibiting degranulation of preoxidase-containing granules by macrophates.
The persistance of intra-macrophage brucella in Undulant Fever results in?
Granuloma formation in the spleen, liver, bone marrow, lymph nodes, and kidneys.
What causes the most severe form of Undulant fever?
B. melitensis

B. suis is next most severe

Fatalities are low, and generally due to endocarditis
What is the treatment for Brucellosis?
Doxycycline and Rifampin (4-6 weeks)

Trimethoprim-sulfamethoxazole instead of doxycycline in pregnant women and children
Pasteurization of milk helps prevent the spread of what zoonotic disease?
How is Brucellosis prevented?
Animal vaccination
Pasteurization of milk
What are the three major species of Yersina?
Yersina pestis
Yersina enterocolytica
What grouping do Yersina fall into?
Enterobacteriaceae, gram negative, pleomorphic rods, facultative anaerobe, facultative intracellular pathogen, optimal growth at 28 C is?
Yersina pestis
What is the vector for Yersina pestis?
The rat flea
What are the two types of plague caused by Yersina, and what are their incubation times?
Bubonic plague - exposure from rat flea. 2-6 day incubation

Pneumonic plague - exposure from person to person. 1-3 day incubation
What are the important virulence factors of Yersina?
Low Calcium Response - lcr - Plasmid gene that allows the organism to grow in low Ca++ intracellular environment. Also coordinates production of other virulence factors, such as V, W, and yops.

V and W proteins - Plasmid coded proteins associated with rapid proliferation and septicemia

Yops - Group of 11 proteins coded on plasmids that are essential for rodent pathogenesis and responsible for cytotoxicity, inhibition of phagocyte migration and engulfment, and platelet aggregation.

Envelope (F1) antigen - Protein-polysaccharide that is highly expressed at 37 degrees in host but not in flea

Coagulase - micro thrombi

Plasminogen Activator - Dissemination and destroys C3b on surface
What are the manifestations of plague?
Malaise, high fever, enlarged lymph nodes which may progress to buboes.

Intermittent septicemia initially, then rapidly becomes constant.


Diffuse hemorrhagic changes + cyanosis from necrotizing pneumoniae - gives name "black death"

Endotoxic shock
What stain is used for Yersina?
Giesma stain
What are the mortality rates for treated and untreated Yersina infections?
~90% for Bubonic plague
100% for septicemic or Pneumonic plague

5-20% mortality with treatment.
What is the drug of choice for Yersina?
Streptomycin, often in combination with chloramphenicol

Beta-lactams are not useful
Yersina enterocolitica disease presents as?
Diarrhea and/or vomiting fever with abdominal pain.
Gram negative, rod, motile at 25 C but nonmotile at 37 C, able to invade mammalian cells is?
Yersina enterocolitica
How is Yersina enterocolitica disease identified?
Stool culture

Growth on CIN media at 25 and 37 C with cold enhancement techniques

Biochemical and serological identification

Agglutination titers
What is primary treatment for Yersina enterocolitica disease?
Care is primarily supportive, as antibiotics do not influence the course of uncomplicated enteritis
What is the causative agent of tularemia?
Francisella tularensis
Non-motile, non-spore forming, gram negative, cocco-bacillus found in diverse animal hosts is?
Grancilla tularensis
What were the two (best known) investigated Bioweapons?
Bacillus Anthracis - Anthrax

Francisella Tularensis - Tularemia
What are the biovars of F. tularensis?
Type A - Highly virulent in humans and animals, most common in N. America

Type B - Relatively avirulent, thought to cause all human tularemia in Europe and Asia
What are the modes of infection for F. tularensis?
MANY MANY - Highly infective, low infectious dose: 10-50 organisms

Handling contaminated animal tissues or fluids

Bite of infective deer flies, mosquitoes, ticks

Contact/Ingestion of contaminated water, food, soil

Inhalation of infective aerosols
How many cases of tularemia are there per year in the US? When and where are they located?
About 200 cases a year

Mostly in south-central and western states, in rural areas occurring in the summer.
What are the types of tularemia and associated mortality rates?
Treated mortality - 1-3%

Untreated mortality:
30-60% for pneumonic
5% for ulceroglandular
Where for F. tularensis replicate?
Inside macrophages
What are the clinical forms of F. tularensis disease?
Ulceroglandular - Ulcer at inoculation site with regional adenopathy

Glandular - Regional adenopathy without skin lesion

Oculoglandular - Painful purulent conjunctivitis with regional adenopathy

Pneumonic - Primary from aerosol exposure or secondary from bacteremia
What are the clinical features of F. tularensis?
General – high fever, malaise, myalgia, headache, chills and rigors, sore throat

Respiratory - dry/slightly productive cough

Gastrointestinal - nausea, vomiting, diarrhea
What do you use to grow F. tularensis?
Blood agar with cysteine supplementation

All growth and identification is performed at designated reference labs, due to high risk of exposure to technicians
What is the treatment for F. tularensis? How is infection controlled?
Adults - Streptomycin, Gentamicin

Pregnant women - Gentamycin preferred over Streptomycin

***No patient isolation necessary due to lack of human-to-human transmission
What are the prophylaxis options for F. tularensis?
A vaccine is under FDA review

For known aerosol exposure, 14 day oral antibiotic regimen

In covert attack situation, observe for development of fever for 14 days, and treat with antibiotics of febrile

Post-exposure antibiotics are most effective when given within 24 hours of exposure
Gram negative, nonmotile, bipolar staining, coccobacillus, Oxydase positive, Catalase positive, AAF, that grow small non-hemolytic colonies on blood agar is?
Pasteurella multocida
What are the capsular types of P. multocida?
Pasteurella moltocida

Capsular types A, B, D, and E

A - most human and fowl isolates
B - most cattle isolates
How does human infection with P. moltocida occur?
Results from dog or cat bites
What is the pathogenesis of P. moltocida disease?
Infection in subcutaneous tissues causes severe local abscesses, which spread to local lymph nodes.

Abscesses require surgical drainage.
What is the treatment for P. moltocida?

Therapy may be prolonged, as abscesses resolve slowly.

Vaccines are not available for humans
How does P. moltocida grow on blood agar?
Small, nonhemolytic colonies