ICL 2.12: Corynebacterium & Actinomycetes Flashcards

Question

what are the effects of the diphtheria toxin on the body?

Answer 1

the diphtheria toxin is absorbed into the mucus membrane and can cause destruction of epithelium and inflammation the necrotic epithelium becomes embedded with fibrin and red/white cells which results in grayish pseudomembrane that is the hallmark of diphtheria C. diphtheriae can then invade and establish in the epithelial layers here, it continues to produce toxin that is readily absorbed and travel to distant tissues this can lead to damage of cardiac, nervous tissue, kidney, liver and adrenals -- damage/hemmorrhage of these tissues can lead to death

Answer 2

the diphtheria toxin is encoded by a lysogenic bacteriophage bacteriophage = a virus that parasitizes a bacterium by infecting it and reproducing inside it only strains infected by this phage can produce toxin and cause diphtheria

Answer 3

initial treatment of diphtheria should be instituted based on clinical diagnosis rather than laboratory tests, since need to act quickly so you base the initial treatment on epidemiologic and clinical clues like if they're non-vaccinated and/or have visited endemic areas even though C. diphtheriae has some characteristic growth and morphology features, they are not reliable for diagnosis

Answer 4

1. selective media include cysteine-tellurite blood agar = CTBA or Tinsdale; best to diagnose 2. colistin-nalidixic agar = CNA; allows growth, but not diagnostic Tellurite inhibits most respiratory tract and Gram-negative bacteria C. diphtheriae reduce tellurite to form gray-black color on agar

Answer 5

most important assay is for production of diphtheria toxin or possess phage 1. Elek test was used historically to detect toxin -- see precipitate formed when toxin binds to antitoxin PCR tests for presence of tox gene -- Get false positive if toxin not expressed

Answer 6

the most important treatment for diphtheria is early administration of antitoxin -- it's most effective when administered within 3 days of disease development but it can't neutralize toxin that has already entered host cells Equine diphtheria antitoxin (DAT) is the mainstay of treatment!! but you have to perform sensitivity test before administering horse serum to prevent serum sickness you also need to make sure airway is clear since pseudomembrane can extend into the nasopharnyx or down the larnyx and swelling of lymphatics in neck can also occlude breathing

Answer 7

1. prevent further exotoxin production 2. prevent carrier status penicillin or erythromycin is DOC

Answer 8

yup there's an extremely effective and safe vaccine is available for preventing diphtheria

Answer 9

it's actually a diphtheria and tetanus toxoids and accellular pertusis vaccine = DTaP 4 doses needed initially and then another final dose around 4-6 years old

Answer 10

1. DTaP | 2. Tdap

Answer 11

combined vaccine against diphtheria, tetanus, and pertussis -- pertussis component is acellular children receive 4 doses at normal or “catch-up” schedule the acellular vaccine is safer to administer and there's fewer side-effects, such as local pain and redness, and/or fever

Answer 12

acronym for the collective vaccines preventing tetanus, diphtheris, and pertussus in adolescents and adults differ from the childhood DTaP vaccines in that the concentration of diphtheria and pertussis toxoid has been reduced (lowercase d and p) it's the booster for “adolescents” and “adults” of all ages who have already received the initial vaccine series -- given every 10 years can be given more frequently in certain situations like a pertussis outbreak or if in the catch up program

Answer 13

MICROBIOLOGY: Gram + pleomorphic rods, facultative anaerobe, non-motile, short-chain mycolic acid in cell wall, grow in clumps (Chinese letters), contain metachromatic granules PATHOLOGY: Causes diphtheria. Start in nasal cavity. Gradual onset. Production of binary toxin encoded by bacteriophage that terminates protein synthesis and kills cells. Toxin causes formation of pseudomembrane in throat-associated tissues. Dead tissue provides environment for bacteria to grow and release more toxin, and may block breathing. Initial illness is mild with sore throat, but progresses to severe as toxin affects heart, nervous tissue, kidney, liver, and adrenals. EPIDEMIOLOGY: Can live in throat without causing disease. Even vaccinated can be carrier, since antibodies are against toxin, not actual bacteria. Most cases seen in countries with poor vaccine coverage, but visitors can pick up and carry back to affect unvaccinated in developed countries. CLINICAL: Initial illness is mild with sore throat. See formation of pseudomembrane in throat tissues 2-3 days after symptoms start, which can block breathing, but also a site for bacterial growth. As toxin spreads, see severe symptoms heart, nervous tissue, kidney, liver, and adrenals. Often fatal. DIAGNOSIS: Initial treatment is quickly initiated based on clinical symptoms and epidemiology. Bacteria growth on cysteine-tellurite blood agar (CTBA or Tinsdale) is selective and best to diagnose. CAN agar allows growth, but not diagnostic. Can perform Elek test to detect toxin or use PCR to identify the presence of the toxin gene (but not proved toxin is being produced). TREATMENT: Most important is early administration of antitoxin to neutralize effects. Also, must assess pseudomembrane to prevent patient choking. DTaP vaccine is very effective. Penicillin or erythromycin is DOC

Answer 14

1. C. jeikeium 2. C. urealyticum 3. C. amycolatum 4. C. ulcerans 5. C. pseudotuberculosis

Answer 15

opportunistic in immunocompromised patients -- uncommon in healthy people seen on skin of hospitalized patients (40%) regardless of immune status VERY RESISTANT to antibiotics

Answer 16

uncommon in healthy people strong urease producer forms struvite calculi or renal stones risk factors = immunosuppression, genitourinary disorders, urologic procedure, antibiotic therapy resistant to most antibiotics

Answer 17

found on the skin but not oropharynx opportunistic pathogen most commonly isolated Corynebacterium in clinical specimens but often misidentified resistant to many antibiotics

Answer 18

can carry the diphtheria gene disease indistinguishable from diphtheria

Answer 19

can carry the diphtheria gene rare cause of infection

Answer 20

irregularly shaped gram + rods both colonizer and pathogen

Answer 21

1. Pharyngitis (similar to Streptococcus) 2. Wound infections (polymicrobic) 3. Endocarditis, septicemia

Answer 22

penicillin or erythromycin

Answer 23

skin colonizer cheeselike odor in culture causes malodorous feet in colonized people septicemia, osteomyelitis, foreign body infections labs = rod-shaped when young, coccoid when old

Answer 24

resistant to beta lactams, clindamycin, ciprofloxacin DOC = vancomycin, tetracycline, gentamicin

Answer 25

oropharynx and URT

Answer 26

gram positive coccoid grows in clusters!

Answer 27

very mucoid and sticky adheres well to damaged heart valves and causes endocarditis major cause of bacteremia, endophthalmitis, catheter-related infections, CNS infections, pneumonia, peritonitis, and septicemia

Answer 28

unpredictable activity against antibiotics susceptibility testing is necessary for effective treatment

Answer 29

gram positive rods difficult to gram stain

Answer 30

tropheryma whippelii

Answer 31

infects macrophages and persist in host tissues can not be grown outside of host cells!! there are “foamy” macrophages that infiltrate many tissues

Answer 32

men 48-54 years old caucasian

Answer 33

initially seen as GI disorder or arthritis = malabsorption, weight loss, diarrhea, joint pain deposits of fatty acids in intestine and mesenteric lymphatic tissue can also affect bone/joint disorders, neurological manifestations, and CV involvement can also cause disease in other tissues like heart, lung, brain, joint, eye

Answer 34

disease is caused by disordered immune response to persistent bacteria there is increased incidence in certain MHC haplotypes

Answer 35

untreated patients have a poor prognosis it's almost universally fatal after 1 year unless receive the correct diagnosis and therapy

Answer 36

diagnosis is usually by intestinal biopsy 1. PAS-positive macrophage inclusions (not good indicator) 2. IHC staining of bacteria in tissues 3. PCR confirmation of T. whippelii DNA is best!

Answer 37

2 weeks ceftriaxone 1 year + oral trimethoprim-sulfamethoxazole however, you often see relapses

Answer 38

small non-motile grampositive rods grow in short chains or clumps anaerobic they ferment carbohydrates to make propionic acid

Answer 39

commonly found on skin, eyes, ear, oropharynx, and female genital tract often seen as contaminants in blood cultures

Answer 40

1. P. acnes - acne vulgaris | 2. P. propionicum = opportunistic infections

Answer 41

associated with endodontic abscesses and lacrimal canaliculitis (tear duct)

Answer 42

acne vulgaris is a common skin disease most common in adolescents on the face and upper neck it's associated with increase in male sex hormones but it's seen in both males and females it's literally super gross cystic looking acne....

Answer 43

P. acnes can infect and block the sebaceous follicles the bacteria thrive in this less aerobic conditions there's increased sebum and androgen production which causes leukocytes to migrate into the area and create an inflammatory lesion -- this can lead to scaring

Answer 44

1. acne is best managed by topical antibiotics in severe cases = erythromycin, clindimycin, tetracyclines but we're seeing increased antibiotic resistance so.... 2. another option is benzoyl peroxide which increases skin turnover and helps clear pores (doesn't generate resistance) 3. hormonal treatments can also be effective

Answer 45

they grow on most media prefer low oxygen takes 2-5 days to grow

Answer 46

aka nocardia gram + more on the side of nontoxic, invasive and damage from the immune system

Answer 47

a group of Gram-positive bacteria with filamentous growth patterns Individual members of this group can be referred to as an “actinomycete” These bacteria can include the genera Nocardia, Actinomyces, Streptomyces, etc.

Answer 48

an individual genus within the “actinomycetes” group is distinct from Nocardia and Streptomyces

Answer 49

1. aerobic gram + filamentous rods = nocardia | 2. anaerobic gram + filamentous rods = actinomyces

Answer 50

produce medium-chain mycolic acids in cell wall partially acid-fast beading pattern in Gram stain ex. nocardia

Answer 51

do NOT contain mycolic acids in cell wall are NOT acid-fast gram stain is uniform ex. actinomyces

Answer 52

1. nocardia = aerobic gram + filamentous rods nocardia spp. are typically found in the external environment like soils, water, dust or vegetation; not usually found on human skin infections are usually EXOGENOUS 2. actinomyces = anaerobic gram + filamentous rods actinomyces spp. are normally found in mucous membranes of healthy individuals -- especially common in URT infections are usually ENDOGENOUS = a disease arising from an infectious agent already present in the body but previously asymptomatic

Answer 53

all are aerobic gram-positive rods!! filamentous growth -- resemble fungal hyphae but has bacterial cell wall components beaded gram staining (literally looks like beads)

Answer 54

short mycolic acids and other waxes stains weakly acid-fast which distinguishes it from actinomyces which are NOT acid fast and stain uniformly

Answer 55

grows on most lab media takes 3-5 days colonies range from white to orange

Answer 56

exogenous! aka come from the environment

Answer 57

1. pulmonary disease 2. brain abscess 3. primary cutaneous infections after trauma 4. subcutaneous infections

Answer 58

usually in immunocompromised patients or patients with existing lung disease can spread hematogenously from lungs to infect other tissues (brain and skin)

Answer 59

happens in 30% of patients with Nocardia infection common in patients with T cell deficiencies like AIDS can present initially as chronic meningitis

Answer 60

mycetoma (feet) cellulitis

Answer 61

a subcutaneous infection that can result from nocardia infections it's a chronic subcutaneous infection often caused by anaerobic actinomycetes or fungi but can also be seen with nocardia actinomycetes more common than fungi usually in the food or lower leg this is different from actinomycosis which is uaully in the cervical-facial, thoracic and pelvic sites looks like super messed up warts on feet

Answer 62

once infection is established, can be quite invasive the bacteria can avoid phagocyte killing by: 1. producing cord factor = prevents phagosome-lysosome fusion 2. prevent acidification of phagolysosome 3. protected from toxic oxygen metabolites = catalase and superoxide dismutase 4. avoid acid phosphatase-mediated killing by using host enzymes as nutrient source

Answer 63

1. staining of sputum, abscess, or CSF samples is the best and fastest method filamentous cells will stain gram + but spotty they will also stain weakly acid-fast (*actinomyces do NOT stain acid-fast) ID at species level requires PCR analyses

Answer 64

will grow on most laboratory media you'll see raised and white-orange colonies takes 3-5 days to grow

Answer 65

antibiotic treatment should be 6 weeks or more for disseminated disease treat local infection with trimethoprime-sulfamethoxazole treat disseminated infections with combined drugs = Amikacin and a carbapenem (e.g. Imipenem)

Answer 66

all are anaerobic Gram-positive rods filamentous growth that resembles fungal hyphae but has bacterial cell wall components gram stain appears normal

Answer 67

cell wall structure LACKS mycolic acids is NOT acid-fast which is what distinguishes it from nocardia

Answer 68

growth on laboratory media requires anaerobic conditions can take 2 weeks or more for growth colonies appear white to yellowish and have domed irregular surface that resembles the top of a molar tooth (literally) you DON'T really see hyphael growth which also differs it from nocardia sulfur granules morphology is not normally seen in plate-cultured isolates

Answer 69

organisms normally colonize humans upper respiratory, GI, and female genital tract NOT normally found on skin

Answer 70

infections caused by endogenous organisms poor oral hygiene or dental procedures aspiration into lungs GI surgery or trauma to bowels abdominal infection or IUD can lead to pelvic infection lung infection can spread to CNS

Answer 71

1. A. naeslundii 2. A. radingae 3. A. turicensis 4. A. israelii

Answer 72

1. cervicofacial 2. thoracic 3. abdomen and pelvis 4. cutaneous/subcutaneous infections can occur 5. brain abscesses can occur, but rare

Answer 73

most common (50-70% of cases) history of dental manipulation or trauma to the mouth, poor oral hygiene, dental caries, or periodontal disease acute pyogenic disease or slowly evolving painless process “lumpy jaw” in humans and animals

Answer 74

15-20% of cases pulmonary infiltrate or mass that can spread to involve the pleura, pericardium, and chest wall

Answer 75

10-20% of cases history of recent or remote bowel surgery, or ingestion/insertion foreign body carrying bacteria presents as slow growing tumor

Answer 76

is the most common form of hypersensitivity pneumonitis -- reactivity to Actinomyces are the major cause of Farmer’s lung inflammation of lungs due to breathing in a foreign substance like dust, fungus, molds etc. initial exposure causes sensitization and subsequent exposures produces hypersensitivty reaction = type III hypersensitivity response sensitized persons have antigen-specific Abs and C3b deposition is observed the reaction produces large neutrophil and lymphocyte influx and large amounts of inflammatory cytokines and prolonged inflammation

Answer 77

1. Acute disease occurs after large exposure. there's an onset of fever, chills, non-productive cough, chest tightness, dyspnea, headache, and malaise 2. subacute disease manifests as chronic cough, dyspnea, anorexia, & weight loss -- is insidious in onset and may occur over weeks to months 3. chronic disease results from extended exposure to the antigen --> can lead to irreversible lung damage, severe dyspnea and dramatic weight loss

Answer 78

actinomyces

Answer 79

laboratory confirmation of actinomycosis is often difficult because all sample types can be contaminated by normal flora also organisms recovered from abscess can be sparse or concentrated in sulfur granules “Sulfur granule” cluster of bacteria should be crushed, stained, and assessed microscopically thin branching rods along granule periphery will stain Gram+ --> actinomyces do not stain acid fast! ID at species level requires biochemical/PCR analyses

Answer 80

they are fastidious and grow slowly under anaerobic conditions takes 2 weeks or more to grow you'll see raised white-yellow colonies

Answer 81

pathogenic actinomyces are susceptible to penicillin treat for 6 months to 1 year should also drain abscess or surgically debride involved tissues they are resistant to metronidazole, aminoglycosides, aztreonam, co-trimoxazole (TMP-SMX), penicillinase-resistant penicillins (eg, methicillin, nafcillin, oxacillin, cloxacillin), and cephalexin