Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
143 Cards in this Set
- Front
- Back
|
What kind of parasite is Chlamydia and why?
|
Obligate intracellular parasite
Cannot synthesize own ATP, must acquire from host via ATP translocase |
|
|
How can chlymydia be grown in culture?
|
On embryonated eggs or in tissue culture
|
|
|
What is the structure of the Chlamydia cell wall?
|
Rigid cell wall, no peptidoglycan, does have LPS
|
|
|
What is the life cycle of Chlamydia?
|
Elementary body persists in environment (metabolically inactive) --> invades a cell --> forms an inclusion body inside a cell --> transforms into metabolically active reticulate body
|
|
|
What are the 3 major species of Chlamydia that are significant to humans? Disease associations?
|
C. Pneumoniae = walking pneumonia, transmitted person to person
C. psittaci = found in birds, causes pneumonia in bird owners C. trachomatis = STDs --> nongonococcal urethritis, cervicitiis, PID Also causes neonatal disease, ocular disease |
|
|
What does Rickettsia look like?
Gram? |
Small, pleomorphic coccobacili
Gram negative structurally, but does not stain |
|
|
What is the structure of the wall of Rickettsia?
|
Has LPS and peptidoglycan
|
|
|
What kind of parasites are Rickettsia?
2 places they can grow ex vivo? |
Obligate intracellular
Yolk sac of embryonated eggs or tissue culture |
|
|
Where does Rickettsia replicate?
|
Endothelial cells of blood vessels --> cell damage --> local inflammation and bleeding
|
|
|
How is Rickettsia transmitted?
2 major groups? |
Arthropod vector (specific for each species of Rickettsia) associated with specific host and specific geography
Rocky Mountain Fever Typhus |
|
|
What kind of parasite is Chlamydia and why?
|
Obligate intracellular parasite
Cannot synthesize own ATP, must acquire from host via ATP translocase |
|
|
What kind of parasite is Chlamydia and why?
|
Obligate intracellular parasite
Cannot synthesize own ATP, must acquire from host via ATP translocase |
|
|
How can chlymydia be grown in culture?
|
On embryonated eggs or in tissue culture
|
|
|
How can chlymydia be grown in culture?
|
On embryonated eggs or in tissue culture
|
|
|
What is the structure of the Chlamydia cell wall?
|
Rigid cell wall, no peptidoglycan, does have LPS
|
|
|
What is the structure of the Chlamydia cell wall?
|
Rigid cell wall, no peptidoglycan, does have LPS
|
|
|
What is the life cycle of Chlamydia?
|
Elementary body persists in environment (metabolically inactive) --> invades a cell --> forms an inclusion body inside a cell --> transforms into metabolically active reticulate body
|
|
|
What is the life cycle of Chlamydia?
|
Elementary body persists in environment (metabolically inactive) --> invades a cell --> forms an inclusion body inside a cell --> transforms into metabolically active reticulate body
|
|
|
What are the 3 major species of Chlamydia that are significant to humans? Disease associations?
|
C. Pneumoniae = walking pneumonia, transmitted person to person
C. psittaci = found in birds, causes pneumonia in bird owners C. trachomatis = STDs --> nongonococcal urethritis, cervicitiis, PID Also causes neonatal disease, ocular disease |
|
|
What are the 3 major species of Chlamydia that are significant to humans? Disease associations?
|
C. Pneumoniae = walking pneumonia, transmitted person to person
C. psittaci = found in birds, causes pneumonia in bird owners C. trachomatis = STDs --> nongonococcal urethritis, cervicitiis, PID Also causes neonatal disease, ocular disease |
|
|
What does Rickettsia look like?
Gram? |
Small, pleomorphic coccobacili
Gram negative structurally, but does not stain |
|
|
What does Rickettsia look like?
Gram? |
Small, pleomorphic coccobacili
Gram negative structurally, but does not stain |
|
|
What is the structure of the wall of Rickettsia?
|
Has LPS and peptidoglycan
|
|
|
What is the structure of the wall of Rickettsia?
|
Has LPS and peptidoglycan
|
|
|
What kind of parasites are Rickettsia?
2 places they can grow ex vivo? |
Obligate intracellular
Yolk sac of embryonated eggs or tissue culture |
|
|
What kind of parasites are Rickettsia?
2 places they can grow ex vivo? |
Obligate intracellular
Yolk sac of embryonated eggs or tissue culture |
|
|
Where does Rickettsia replicate?
|
Endothelial cells of blood vessels --> cell damage --> local inflammation and bleeding
|
|
|
Where does Rickettsia replicate?
|
Endothelial cells of blood vessels --> cell damage --> local inflammation and bleeding
|
|
|
How is Rickettsia transmitted?
2 major groups? |
Arthropod vector (specific for each species of Rickettsia) associated with specific host and specific geography
Rocky Mountain Fever Typhus |
|
|
How is Rickettsia transmitted?
2 major groups? |
Arthropod vector (specific for each species of Rickettsia) associated with specific host and specific geography
Rocky Mountain Fever Typhus |
|
|
What kind of parasite is Chlamydia and why?
|
Obligate intracellular parasite
Cannot synthesize own ATP, must acquire from host via ATP translocase |
|
|
How can chlymydia be grown in culture?
|
On embryonated eggs or in tissue culture
|
|
|
What is the structure of the Chlamydia cell wall?
|
Rigid cell wall, no peptidoglycan, does have LPS
|
|
|
What is the life cycle of Chlamydia?
|
Elementary body persists in environment (metabolically inactive) --> invades a cell --> forms an inclusion body inside a cell --> transforms into metabolically active reticulate body
|
|
|
What are the 3 major species of Chlamydia that are significant to humans? Disease associations?
|
C. Pneumoniae = walking pneumonia, transmitted person to person
C. psittaci = found in birds, causes pneumonia in bird owners C. trachomatis = STDs --> nongonococcal urethritis, cervicitiis, PID Also causes neonatal disease, ocular disease |
|
|
What does Rickettsia look like?
Gram? |
Small, pleomorphic coccobacili
Gram negative structurally, but does not stain |
|
|
What is the structure of the wall of Rickettsia?
|
Has LPS and peptidoglycan
|
|
|
What kind of parasites are Rickettsia?
2 places they can grow ex vivo? |
Obligate intracellular
Yolk sac of embryonated eggs or tissue culture |
|
|
Where does Rickettsia replicate?
|
Endothelial cells of blood vessels --> cell damage --> local inflammation and bleeding
|
|
|
How is Rickettsia transmitted?
2 major groups? |
Arthropod vector (specific for each species of Rickettsia) associated with specific host and specific geography
Rocky Mountain Fever Typhus |
|
|
Rocky Mountain Spotted Fever
a. Reservoir b. Transmitted by? c. Incubation time d. Symptoms e. Species implicated |
a. Rodents
b. Ticks c. 1 week d. Fever, myalgias, headache --> rash after 1 week e. Rickettsia rickettsii |
|
|
Typhus
a. Species implicated b. Reservoir c. Transmission |
a. Rickettsia prowazekii
b. Areas with poor hygeine, and crowding, possibly animals c. Human body louse |
|
|
Rocky Mountain Spotted Fever
a. Reservoir b. Transmitted by? c. Incubation time d. Symptoms e. Species implicated |
a. Rodents
b. Ticks c. 1 week d. Fever, myalgias, headache --> rash after 1 week e. Rickettsia rickettsii |
|
|
What do Erlichia and Anaplasma look like?
Gram? |
Small cocci
Similar to gram negative (double membrane cell wall) but no LPS or peptidoglycan |
|
|
Typhus
a. Species implicated b. Reservoir c. Transmission |
a. Rickettsia prowazekii
b. Areas with poor hygeine, and crowding, possibly animals c. Human body louse |
|
|
With what do Ehrlichia and Anaplasma stain?
|
Wright or Giemsa stain
Not gram stain |
|
|
What do Erlichia and Anaplasma look like?
Gram? |
Small cocci
Similar to gram negative (double membrane cell wall) but no LPS or peptidoglycan |
|
|
What type of parasite is Ehrlichia/Anaplasma?
How do they infect? |
Obligate intracellular
grow in membrane bound vacuoles of leukocytes --> form intracellular microcolonies called morulae |
|
|
With what do Ehrlichia and Anaplasma stain?
|
Wright or Giemsa stain
Not gram stain |
|
|
Ehrlichia chaffeensis
a. Where does it grow b. What does it cause c. What is the vector? d. What is the reservoir? |
a. Grows in monocytes
b. Human monocytic ehrlichiosis c. ticks d. Rodents |
|
|
What type of parasite is Ehrlichia/Anaplasma?
How do they infect? |
Obligate intracellular
grow in membrane bound vacuoles of leukocytes --> form intracellular microcolonies called morulae |
|
|
Anaplasma phagocytophilum
a. What type of cell does it infect b. What does this cause c. Transmitted by? d. Reservoir? e. Disease association |
a. Infects granulocytes, PMNs
b. Granulocytic ehrlichiosis c. Ticks d. Rodents e. Acute febrile syndrome with blood cell abnormalities |
|
|
Ehrlichia chaffeensis
a. Where does it grow b. What does it cause c. What is the vector? d. What is the reservoir? |
a. Grows in monocytes
b. Human monocytic ehrlichiosis c. ticks d. Rodents |
|
|
What type of pathogen is Q fever?
What can it be cultured in/on? |
Obligate intracellular
Cultured on embryonated eggs or tissue culture |
|
|
Anaplasma phagocytophilum
a. What type of cell does it infect b. What does this cause c. Transmitted by? d. Reservoir? e. Disease association |
a. Infects granulocytes, PMNs
b. Granulocytic ehrlichiosis c. Ticks d. Rodents e. Acute febrile syndrome with blood cell abnormalities |
|
|
What type of membrane does Q fever have?
|
Gram negative membrane, but does not stain with gram stain
|
|
|
What type of pathogen is Q fever?
What can it be cultured in/on? |
Obligate intracellular
Cultured on embryonated eggs or tissue culture |
|
|
What is phase variation in Q fever?
|
Q fever organism has two antigen types (phase I and II) caused by switching of the expression of LPS genes
|
|
|
What type of membrane does Q fever have?
|
Gram negative membrane, but does not stain with gram stain
|
|
|
What is phase variation in Q fever?
|
Q fever organism has two antigen types (phase I and II) caused by switching of the expression of LPS genes
|
|
|
Q fever
a. Reservoir b. Transmission c. How do humans acquire |
a. Cattle, sheep, goats
b. Ticks c. inhalation |
|
|
What happens in acute Q fever infection?
|
Acute: Self-limited pneumonia/pulmonary syndrome, with fever, chills, headache, fatigue, sweats, muscle ache
|
|
|
What happens in chronic Q fever infection?
What if pregnant women are infected with Q fever? |
Endocarditis
Abortions, neonatal deaths |
|
|
How is the cell wall of mycoplamsa unusual?
How does this affect effective drugs? |
No cell wall (so no peptidoglycan, no outer membrane, no capsule) -- only plasma membrane in their cell envelope
Drugs targeting cell wall ineffective (B-lactams, vancomycin) |
|
|
What type of parasite is mycloplasma?
|
Obligate
Require sterols for growth, incorporate cholesterol into their plasma membrane for stability |
|
|
Where do mycoplasmas attach and how?
|
Attachment structure at tip:
P1 adhesin binds to respiratory epithelium --> ciliostasis, local inflammation, tissue destruction --> peroxides liberated |
|
|
What kinds of antibiotics are effective against mycoplasmas?
|
Antibiotics that inhibit protein synthesis
|
|
|
What are 3 main causes of bacterial pneumonia in the US?
|
pneumococcus, chlamydiae, and mycloplasma
|
|
|
What does mycoplasma pneumoniae cause?
|
community-acquired pneumonia
Walking pneumonia, with gradual onset |
|
|
What are the effects of mycoplasma genitalium and ureaplasma urealyticum?
|
Urethritis (nongonococcal)
|
|
|
Why can't spirochetes be seen with gram stain or a normal light microscope?
What do you use instead? |
Too narrow
Use dark field microscopy or silver-based stains |
|
|
What does the wall of spirochetes look like?
|
Inner and outer membrane, peptidoglycan with flagella in periplasmic space
Similar to gram negative structure, but does not gram stain |
|
|
Which species of spirochetes has LPS?
|
Leptospira, signals through TLR 2
|
|
|
How do spirochetes move?
|
Have flagella in their periplasmic space, corkscrew motility
|
|
|
Treponema pallidum
a. How many species b. What type of parasite c. hosts? d. oxygen? e. number needed to cause an infection |
a. 4
b. obligate c. humans d. microaerophilic e. need fewer than 10 |
|
|
What does Treponama pallidum cause?
|
Syphilis
|
|
|
What are the three stages of syphilis?
|
Primary = chancre (painless genital ulcer)
Secondary (3-6 months later) generalized rash, resolves itself Tertiary (after decades of latency) = benign gummatous (skin and bones manifestations), cardiovascular (ascending aortic aneurysm), neurosyphilis |
|
|
What is the treatment of syphillis?
|
Penicillin
|
|
|
What are 2 diseases caused by Borrelia?
What are their species associations? |
Lyme disease - B. burgdorferi
Relapsing fever Endemic = b. hermsii, b. turicatae, b. parkeri Epidemic = b. recurrentis |
|
|
Lyme disease
a. species b. distributed by? |
a. Borrelia burgdorferi
b. tick |
|
|
What does the early stage of lyme disease look like?
Late stage? |
Early = Erythema chronicum migrans - rash; musculoskeletal, cardiovascular, neurological symptoms
Late = arthritis, carditis, neuropathy |
|
|
Endemic Relapsing fever
a. Species (3) b. transmitted by? c. Reservoir d. diagnosis by? |
a. b. hermsii, b. turicatae, b. parkeri
b. soft bodied ticks c. rodent d. blood smear |
|
|
What does the early stage of lyme disease look like?
Late stage? |
Early = Erythema chronicum migrans - rash; musculoskeletal, cardiovascular, neurological symptoms
Late = arthritis, carditis, neuropathy |
|
|
Epidemic Relapsing fever borreliae
a. species b. transmitted by? c. conditions associated with...? |
a. b. recurrentis
b. body louse c. unhygenic environments, warfare |
|
|
Endemic Relapsing fever
a. Species (3) b. transmitted by? c. Reservoir d. diagnosis by? |
a. b. hermsii, b. turicatae, b. parkeri
b. soft bodied ticks c. rodent d. blood smear |
|
|
Why is their a recurrence of fever from borreliae?
|
Different antigenic protein on surface of bacteria each time
|
|
|
Epidemic Relapsing fever borreliae
a. species b. transmitted by? c. conditions associated with...? |
a. b. recurrentis
b. body louse c. unhygenic environments, warfare |
|
|
How are leptospira different from other spirochetes (3)?
|
Larger genome
LPS survives in water |
|
|
Why is their a recurrence of fever from borreliae?
|
Different antigenic protein on surface of bacteria each time
|
|
|
Where is Leptospora primarily a problem? hosts?
|
Tropics and subtropics - mammals
Urban - rats, cattle, dogs |
|
|
How are leptospira different from other spirochetes (3)?
|
Larger genome
LPS survives in water |
|
|
Leptospira infection
a. reservoir b. transmission c. early phase d. late phase |
a. rats, dogs, cattle
b. excreted in urine, contaminates water --> absorbs through skin, mucous membranes c. Bacteremia - nonfocal fever d. Weil's disease - liver failure, kidney failure, pulmonary hemorrhage |
|
|
Where is Leptospora primarily a problem? hosts?
|
Tropics and subtropics - mammals
Urban - rats, cattle, dogs |
|
|
Leptospira infection
a. reservoir b. transmission c. early phase d. late phase |
a. rats, dogs, cattle
b. excreted in urine, contaminates water --> absorbs through skin, mucous membranes c. Bacteremia - nonfocal fever d. Weil's disease - liver failure, kidney failure, pulmonary hemorrhage |
|
|
mycobacteria
a. oxygen b. growth time c. membrane |
a. aerobic
b. slow growing c. Gram positive (sort of): lacks LPS, but DOES NOT STAIN WITH GRAM STAIN |
|
|
What type of stain does mycobacterium respond to?
|
acid-fast stain
|
|
|
mycobacteria
a. oxygen b. growth time c. membrane |
a. aerobic
b. slow growing c. Gram positive (sort of): lacks LPS, but DOES NOT STAIN WITH GRAM STAIN |
|
|
What does the cell wall of mycobacterium look like?
|
Lipid bilayer plasma membrane around cytoplasm
Peptidoglycan No LPS or lipotechoic acids, but instead has carb polymers and fatty acids (mycolic acids) |
|
|
What type of stain does mycobacterium respond to?
|
acid-fast stain
|
|
|
What are mycolic acids?
|
Long chain FAs in the wall of mycobacteria (24 and 60 Carbons)
helps make cell resistant to acid, alkali, organic solvents, and desiccation; promotes survival in the environment, but makes staining tough |
|
|
What does the cell wall of mycobacterium look like?
|
Lipid bilayer plasma membrane around cytoplasm
Peptidoglycan No LPS or lipotechoic acids, but instead has carb polymers and fatty acids (mycolic acids) |
|
|
What is wax D?
Use? |
Mycolic acid + arabinogalactan + peptidoglycan
Induces granuloma formation and caseous necrosis by mycobacteria; can act as adjuvants |
|
|
What are mycolic acids?
|
Long chain FAs in the wall of mycobacteria (24 and 60 Carbons)
helps make cell resistant to acid, alkali, organic solvents, and desiccation; promotes survival in the environment, but makes staining tough |
|
|
What is cord factor?
What effects does it have on various cells? |
allows mycobacteria to stick together
Toxic to PMNs, damages mitochondira, causes granulomas |
|
|
What is wax D?
Use? |
Mycolic acid + arabinogalactan + peptidoglycan
Induces granuloma formation and caseous necrosis by mycobacteria; can act as adjuvants |
|
|
What is cord factor?
What effects does it have on various cells? |
allows mycobacteria to stick together
Toxic to PMNs, damages mitochondira, causes granulomas |
|
|
How are mycobacteria stained (4 steps)?
What is the result? |
1. Heat fix specimen to slide
2. Stain with boiling carbol fuchsin 3. Decolorize with 95% ethanol and 3% HCl (myobacterium resist this step) 4. Counterstain with methylene blue Blue background, red mycobacteria |
|
|
How are mycobacteria stained (4 steps)?
What is the result? |
1. Heat fix specimen to slide
2. Stain with boiling carbol fuchsin 3. Decolorize with 95% ethanol and 3% HCl (myobacterium resist this step) 4. Counterstain with methylene blue Blue background, red mycobacteria |
|
|
M. tuberculosis
a. reservoir b. transmission |
a. Humans, cattle (m. bovis)
b. Person to person, inhalation of droplets (1-5 microns) Ingestion via dairy products from infested cows as well |
|
|
M. tuberculosis
a. reservoir b. transmission |
a. Humans, cattle (m. bovis)
b. Person to person, inhalation of droplets (1-5 microns) Ingestion via dairy products from infested cows as well |
|
|
What type of pathogen is M. tuberculosis?
How does it act? |
Intracellular
Engulfed by macrophages, lives in phagosome (resistent to ROS), prevents phagolysosomal fusion --> drain to lymph nodes --> multiply --> bacteremia |
|
|
What type of pathogen is M. tuberculosis?
How does it act? |
Intracellular
Engulfed by macrophages, lives in phagosome (resistent to ROS), prevents phagolysosomal fusion --> drain to lymph nodes --> multiply --> bacteremia |
|
|
On what factors does the primary infection of m. tuberculosis depend?
|
1. Number of organisms
2. Resistance of host |
|
|
On what factors does the primary infection of m. tuberculosis depend?
|
1. Number of organisms
2. Resistance of host |
|
|
What are 2 types of lesions caused by tuberculosis?
|
1. Exudative = acute inflammation (PMNs, edema)
2. Granulomatous = later, 3 zones -central zone = giant cells midzone = epithelioid cells outer zone = fibroblasts, monocytes, lymphocytes |
|
|
How does the primary disease of tuberculosis play out?
|
most people are asymptomatic, mild respiratory infection
|
|
|
What is reactivation disease of tuberculosis?
|
After a latent tuberculosis infection, reactivation occurs (most often in lungs) --> symptomatic, can be serious
|
|
|
What are 4 methods for diagnosis of tuberculosis?
|
1. Skin testing
-inject PPD, tuberculin --> look for delayed-type hypersensitivity 2. Quantiferon - look for IFN-gamma after m. tuberculosis antigens 3. Acid-fast staining 4. Molecular techniques - PCR |
|
|
What are 2 first line agents for TB?
What is the typical regimen for pulmonary TB |
Isonazid, Refampin, ethambtol, pyrazinamide
4 drugs for 2 months, then 2 drugs for 4 months |
|
|
What is Multidrug resistant tuberculosis?
|
resistent to at least two first line agents, usually isonazid and rifampin
|
|
|
What are Extremely drug resistant TB strains resistant to?
|
First line = Isonazid, rifampin, fluoroquinolone
At least one second line drug |
|
|
What are the classifications of nontuberculous mycobacteria?
|
Group 1 - photochromogens - produce pigment when grown in light only
Group 2 - Scotochromogens - produce pigment in light or dark Group 3 - Nonchromagens - no pigment Group 4 - Rapid growers |
|
|
What are 3 examples of Group 1 photochromogens?
|
M. kansasii - TB-like syndrome
M. marinum - skin and soft tissue infections when exposed to water M. ulcerans - buruli ulcer |
|
|
What is one example of a group 2 scotochromogen?
|
M. scrofulaceum - cervical adenitis in children
|
|
|
What are Group 4 nontuberculous mycobacteria?
What are 2 species? |
Rapid growers (within 7 days), variable pigmentation, don't usually cause infection
M. fortuitum, and M. abscessus-chelonae |
|
|
What are the 2 major groups of group 3 non-tuberculous mycobacterium?
|
1. m. avium
2. m. intracellulare |
|
|
What are 2 major disease syndromes associated with mycobacterium avium complex?
|
1. Lung disease (like chronic pulmonary tuberculosis) in patients with preexisting lung disease
2. Nonfocal fever and wasting in immunocompromised patients (AIDS) --> bacteremia, growth in nodes, liver, lung, marrow |
|
|
M. leprae
a. staining b. how related is it to m. tuberculosis c. transmission d. incubation |
a. acid fast
b. 44% same as m. tuberculosis c. spread by respiratory or direct contact d. incubation 2-10 years |
|
|
How does the WHO classify disease of m. leprae
|
Classifies by number of sites and number of organisms at each site
Classifies as paucibacillary or multibacillary |
|
|
How does the Ridley-Jopling classification of m. leprae work?
|
Spectrum of categories which reflect the immunological reaction of the organism
2 most important = tuberculoid and lepromatous |
|
|
Tuberculoid m. leprae
a. T cell response b. skin lesions c. amount of bacteria |
a. Stronger T cell response
b. fewer skin lesions, localized c. Paucibacillary |
|
|
Lepromatous m. leprae
a. T cell response b. skin lesions c. amount of bacteria |
a. No T cell response
b. many nodular lesions c. multibacillary |
|
|
How can one make a diagnosis of m. leprae infection?
|
Skin scraping --> acid fast stain
Biopsy of nerves Skin test using lepromin |
|
|
What are 2 treatments for M. leprae
|
Dapsone (sulfone)
Rifampin and clofazimine (for multibacillary) |
|
|
Nocardia
a. Morphology b. Growing time c. staining |
a. filamentous, branching
b. slow growing c. weakly acid fast because of shorter chain mycolic acids |
|
|
Nocardia
a. Reservoir b. Infections |
a. soil
b. Infect immunocompromised patients --> subacute to chronic pneumonia skin disease |
|
|
What are the antibiotics of choice for nocardia infection?
|
Trimethoprim-sulfamethoxazole
Duration 6-12 months |
|
|
Acinomyces
a. morphology b. Stain c. oxygen d. speed of growth e. predominant species |
a. Filamentous, branching
b. Gram positive, does not acid fast stain (no mycolic acids) c. Anaerobic or microaerophilic d. Slow growing e. Actinomyces israelii |
|
|
How can actinomyces be distinguished from nocardia and mycobateria?
|
Not acid fast, no mycolic acids
|
|
|
Where do actinomyces normally live?
How does infection occur? |
Part of normal flora of the mouth, GI, GU
Infects immunocompromised, following trauma, foreign bodies |
|
|
How do actinomyces infections play out?
|
Form chronic draining sinuses, slow growing mass of fibrous and inflammatory tissue --> sulfur granules
|
|
|
What are 3 syndromes of actinomyces infection?
|
1. Orocervicofacial - soft tissue mass near mouth --> lumpy jaw
2. Thoracic --> pneumonia after aspiration of oral flora 3. Abdominopelvic --> growing mass around bowel |
|
|
What is the therapy for actinomyces infection?
Time? |
Penicillin, 4-12 months
|
