Bacteriology

Front 1

Clostridium Perfringens
General Info

Back 1

-G+ Rods, very few spores
-Aerotolerant
-5 serologic types (A-E)
*A = major pathogen

Front 2

Clostridium Perfringens
Pathogenesis

Back 2

-Requires low Ox-Red Potential -> muscle damage and poor blood supply
-lack of O2 allows spread and toxin release
-alpha toxin (Phospholipase C) causes most damage (disrupts cell membranes, lyses RBCs, platelets, leukocytes, endothelial cells)
-edema and gas accumulation help spread
*** Increase P, Decrease circulation, Decrease O2 supply, Increase Spread

Front 3

Clostridium Perfringens
Clinical Manifestations

Back 3

-wound infections, food poisoning and enteritis
-gas gangrene (can lead to death)
-clostridal cellulitis-infection of tissue that is already dead
-uterine infection
-septicemia
-food poisoning-> diarrhea, cramps, abdominal pain, vomiting uncommon
-necrotic enteritis-from food, loss of intestinal mucosa with bleeding in stool-can be fatal
-antibiotic associated diarrheal disease

Front 4

Clostridium Perfringens
Epidemiology

Back 4

-ubiquitous
-intestinal tracts of humans and mammals awa soil
-deep laceration or crush wound damaging blood supply and muscle predispose (trauma)
-source is endogenous or exogenous and/or spores

Front 5

Clostridium Perfringens
Diagnosis

Back 5

-early needed by clinical symptoms
-confirm with gram stain and culture
-spores are rare
-Nagler Test for  toxin

Front 6

Clostridium Perfringens
Treatment Control

Back 6

Simple Wound/Cellulitis
-remove necrotic tissue and clean thoroughly
-use antibiotic
-penicillin, chloramphenicol for 2 bac. Inf.
Gas Gangrene
-removal of all infected tissue and Increase doses antibiotics
-hyperbaric O2¬ beneficial->inhibits alpha toxin + growth
-Septicemia-antibiotic therapy
-Food Poisoning- no antibiotics; fluids
-antitoxin use controversial

Front 7

Clostridium Difficile
General Info

Back 7

-G+ rods, Obligate Anaerobe

Front 8

Clostridium Difficile
Pathogenesis

Back 8

-pseudomembranous colitis assoc. w/ use of clindamycin, ampicillin & cephalosporins
-other anaerobic flora eliminated by allowing overgrowth by the bacteria
-begins within days or weeks following therapy

Front 9

Clostridium Difficile
Clinical Manifestations

Back 9

-D, colitis, or pseudomembranous colitis

Front 10

Clostridium Difficile
Epidemiology

Back 10

-source is endogenous or exogenous
-risk factors: antibiotic exposure, older age, female sex, impaired intestinal motility
-varies with degree of hospital contamination

Front 11

Clostridium Difficile
Diagnosis

Back 11

-observe pseudomembrane with colonoscope
-ID toxin B in stools w/ EIA (not +)
-isolation from stools
-Must use a combination of the above for ID

Front 12

Clostridium Difficile
Treatment Control

Back 12

-discontinue use of drug
-maintain fluids + electrolyte balance
-avoid drugs that slow intestinal motility
-vancomycin
-untreated mortality rate of PC is high (27-44%)

Front 13

Clostridium Tetani
General Info

Back 13

-G+ rods
-Obligate Anaerobe
-Drumstick shaped with peritrichous flagella and terminal spore

Front 14

Clostridium Tetani
Pathognesis

Back 14

-trauma lowering Ox-Red potential a predisposing factor
-noninvasive (stays in necrotic tissue)
-symptoms when tetanospasmin (neurotoxin) in blood
-fixes to gangliosides and blocks release of neurotransmitter
-incubation period days to weeks (closer to head = bad)
-lethal dose = 0.13 g
-ascending tetanus -> affects peripheral nerves (confined to extremities)
-descending tetanus -> pass into blood/lymph (abs. by all local nerve endings)

Front 15

Clostridium Tetani
Clinical Manifestations

Back 15

-lockjaw (trismus), muscle stiffness, arching of back
-Complications: Pulmonary, Renal, Cardiac
-takes weeks to run its course
-poor prognosis with injury close to head or onset of first seizure close to injury time
-Tetanus Neonatorum – umbilical cord stump infected soon after birth -> major cause of infant mortality in underdeveloped countries

Front 16

Clostridium Tetani
Epidemiology

Back 16

-sporadic disease
-rare in developed countries
-top 10 in others
-spores in soil

Front 17

Clostridium Tetani
Diagnosis

Back 17

-clinical symptoms
-organism can be recovered from the wound in only 1/3 of cases
-DD -> strychnine poisoning and encephalitis

Front 18

Clostridium Tetani
Treatment Control

Back 18

-pooled human antitoxin
-debridement of wound and removal of foreign object
-Antibiotic for anaerobes
-barbiturates or curare-like agents for spasms
-active immunization with toxoid as a part of DTP
-booster vaccination every 10 years

Front 19

Clostridium Botulinum
General info

Back 19

-G+ rods

Front 20

Clostridium Botulinum
Pathonogenesis

Back 20

-neurotoxin type A->flaccid muscle paralysis ->one of most potent poisons known->binds to receptor sites at NMJ and prevents impulses from passing from motor nerves to muscle fibers by interfering with release of Ach(has been used for therapy in dystonia)
-CN involvement -> problems with eyesight, hearing, speech
-decrease saliva, weakness, descending paralysis with resp. failure

Front 21

Clostridium Botulinum
Clinical Manifestations

Back 21

-CN involvement -> problems with eyesight, hearing, speech
-decrease saliva, weakness, descending paralysis with resp. failure
-fever is rare
-food poisoning -> 24-36 hours get N, V, D and abd pain
-infant botulism -> germination of spores in GI tract, related to intestinal flora for a @ 2wks – 6 months, lethargy, abnormal sleep, decrease suck and gag reflexes, swallowing problems, head control lost and body becomes flaccid, respiratory arrest may occur

Front 22

Clostridium Botulinum
Epidimeology

Back 22

-food-borne
-worldwide in soil and GI of birds, fish and mammals
-humans susceptible to A, B and E
-honey implicate in infant botulism

Front 23

Clostridium Botulinum
Diagnosis

Back 23

-difficult due to symptoms
-look for toxin in feces, serum, vomitus, or food samples
-normal CSF
-Infant Botulism -> failure to thrive, acute infantile polyneuropathy, dehydration
-CDC for testing-mouse neutraliztion test
-isolation and culture on anaerobic medium
-egg yolk agar to demonstrate lipase activity

Front 24

Clostridium Botulinum
Treatment Control

Back 24

-stomach lavage and high enemas
-antitoxin good if used early
-ventilatory assistance maybe
-Infant Botulism -> supportive care, do not use oral antibiotics

Front 25

Actinomyces
General Info

Back 25

-G+ branching bacilli w/ mycelial-like structures
-most species are aerotolerant
-Sulfur granules
-Human pathogens include:
1. A. israelii
2. A. naeslundii
3. A. viscosus
4. A. odontolyticus

Front 26

Actinomyces
Pathonogeneis

Back 26

entry is by the mucosa of the mouth or the lower g.i. tract
-anaerobic growth in deeper tissues-> multiple pyogenic lesions which become joined @ interconnecting sinuses
-contained in granulomatous lesions and within granules in sinus channels

Front 27

Actinomyces
Epidimiology

Back 27

-direct introduction of organism into injured tissue or endogenous infection
-NO case to case transmission
-higher infection rate in men

Front 28

Actinomyces
Diagnosis

Back 28

-microscopic exam to see granules in clinical specimens
-crush granules and look for G+, nonacid-fast bacilli
-culture and BCH tests

Front 29

Proprionibacterium
General Info

Back 29

-G+ bacilli
-anaerobic
-commonly on skin surface
-P. acnes

Front 30

Proprionibacterium
Pathonogenesis

Back 30

-bacterium stimulates an inflammatory response that results in rupture of sebaceous follicles

Front 31

Proprionibacterium
Clinical Manifestations

Back 31

P. acnes causes acne & opportunistic infections

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Front 45

Proprionibacterium
Treatment Control

Back 45

For acne-Topical benzoyl peroxide & erythromycin

Front 46

Bacteriodes Fragilis
General Info

Back 46

G-, bacilli
-part of normal flora
-endotoxin not highly toxic

-pleomorphic, no spores
-can stand prolonged O2
-plasmid-mediated resistance
-most resistant of all anaerobes
- < ox/red potential or GI trauma predispose

Front 47

Bacteriodes Fragilis
Clinical Manifestations

Back 47

-Intraabdominal infection is common->result of fecal matter spilled into peritoneal cavity during surgery, bowel disease, or cancer
-peritonitis and abscess formation

-Path-conditions predisposed to anaerobic infection apply

Front 48

Bacteriodes Fragilis
Epidimiology

Back 48

-endogenous infection
-found in oral cavity, GI tract, vagina and urethra

Front 49

Bacteriodes Fragilis
Diagnosis

Back 49

-foul odor of discharge, tissue necrosis and gas
-gram stain and BCH ID

Front 50

Fusobacterium Nucleatum
General Info

Back 50

1) G-

2)long rods with thin pointed ends (fusiform)
- < ox/red potential or GI trauma predispose

Front 51

Fusobacterium Nucleatum
CLinical Manifestations

Back 51

-seen most commonly in oral infections, lung abscesses, and pleuropulmonary infections
-mixed infection with spirochetes -> Vincent’s Angina and Trench Mouth

Front 52

Fusobacterium Nucleatum
Epidimiology

Back 52

-endogenous infection
-found in oral cavity and urogenital tract
-Some found in GI tract

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Front 61

Pasteurellaceae: Haemophilus
General Info

Back 61

-Small to medium sized G- coccobacilli or rods
-many strains posses capsules

Front 62

Pasteurellaceae: Haemophilus
Pathogenesis

Back 62

-all require either 1 or both growth factors present in the blood:
1. X factor = hematin
2. V factor = NAD

Front 63

Pasteurellaceae: Haemophilus
Epidimiolgy

Back 63

-satellite phenomenon with staphylococci

Front 64

Pasteurellaceae: Haemophilus
Diagnosis

Back 64

-chocolate agar used as a culture medium
-X & V factors released when blood heated and cells lyse

Front 65

Haemophilus Influenzae
General Info

Back 65

- G-, pleomorphic
-6 capsular types (a-f)
-95% of invasive disease by b

Front 66

Haemophilus Influenzae
Pathogenesis

Back 66

-virulence factors: LPS and capsules (PRP – antiphagocytic)
-POE is the respiratory tract

Front 67

Haemophilus Influenzae
Clinical Manifestations

Back 67

-acute pharyngitis
-otitis media and sinusitis
-epiglottitis (acute onset and rapid course)
-bronchitis and pneumonia
-cellulitis
-conjuctivis
-meningitis (type b most common in kids 3 months-2 yrs, uncommon in adults)

Front 68

Haemophilus Influenzae
Epidimiology

Back 68

-droplet transmission
-unencapsulated strains are carried in nasopharynx of 20-50% of asymp. People
-frequency of invasive infection inversely related to age
-infection during first 2 months of life rare due to maternal Abs
-epiglottitis  3-5 years
-meningitis, pyarthrosis, & cellulitis  2 mo-4 yrs
-most frequent cause of bacterial meningitis
-important cause of otitis media and URT infections

Front 69

Haemophilus Influenzae
Diagnosis

Back 69

-gram stain, isolation, BCH ID from CSF, blood, urine and middle ear aspirates
-throat swabs insignificant
-need 1-2 mL of CSF
-organism is very fastidious and dies quickly -> process quickly
-Tests for type b capsular antigens (PRP) in body fluids-> latex agglutination, EIA, CIE

Front 70

Haemophilus Influenzae
Treatment/Control

Back 70

-treat as a medical emergency and start early while testing for resistances
-resistance to ampicillin, chloramphenicol, tetracycline
-cefotaxime/ceftriaxone for meningitis, epiglottiitis or other serious inf.
-URT inf. and bronchitis -> tmp-smz, ampicillin, amoxicillin
-capsular conjugate vaccine against Hib rec. for all kids @ 2 months

Front 71

Haemophilus Aegyptius
General Info

Back 71

- G-, pleomorphic

Front 72

Haemophilus Aegyptius
Clinical Manifestations

Back 72

Purulent conjunctivitis known as “pink eye”

Front 73

Haemophilus Aegyptius
Epidimiology

Back 73

Occurs in hot climates

Front 74

Haemophilus Aegyptius
Treatment/Control

Back 74

Topical sulfonamides

Front 75

Haemophilus Ducreyi
General Info

Back 75

- G-, pleomorphic

Front 76

Haemophilus Ducreyi
CLinical Manifestations

Back 76

-causes chancroid
-> painful ulcer with ragged margin in genitalia and perianal areas
-> painful, suppurative inguinal buboes characteristic in ½ of pts
-> does not cause systemic infection

Front 77

Haemophilus Ducreyi
Epidimiology

Back 77

-transmitted by sex
-frequent in tropics
-uncommon STD in US
-assoc. w/ poor socioeconomic and hygenic conditions
-co-infection with treponema paliidum (syphillis) and HIV

Front 78

Haemophilus Ducreyi
Diagnosis

Back 78

-gram stain of ulcer or bubo aspirate
-chocolate agar w/ vancomycin
-R/O syphyllis by serologic test & darkfield exam
-few 1000 cases per year
-clusters in NY, LA, IL, FL, TX > 90% US cases

Front 79

Pasturella
Treatment/Control

Back 79

Ampicillin or Tetracycline

Front 80

Pasturella
General Info

Back 80

- G- coccobacilli
-P. Multocida and P. canis are the major human pathogens

Front 81

Pasturella
Pathogenesis

Back 81

-localized abscesses associated with cat or dog bites
-especially in wounds that have been sutured

Front 82

Pasturella
CLinical Manifestations

Back 82

-regional lymphadenitis, discoloration, severe local pain and swelling
-2nd most common form is infection of lung with preexcisitng chronic pulmonary disease

Front 83

Pasturella
Epidimioloy

Back 83

-normal flora of many domestic animals
-transmission by a bite
-animal reservoirs are asymptomatic

Front 84

Pasturella
Diagnosis

Back 84

Isolation from clinical specimen, blood, sputum, or exudate from animal bites

Front 85

Bordetella Pertussis
General Info

Back 85

1)G-
2)coccobacilli
3) extremely small
4)obligate aerobes

-Species that most commonly causes serious human infections

-bipolar metachromatic staining

Front 86

Bordetella Pertussis
Pathogenesis

Back 86

-Virulence factors:
1)Filamentous hemagglutinin- promotes binding to cilia->impt. for colonization of airway

2)Pertussis toxin-A-B toxin-> causes death to ciliated cells and increase mucin secretion

Front 87

Bordetella Pertussis
Clinical Manifestation

Back 87

-catarrhal stage: 1-2 wks, mild Sx of uncomplicated URT inf (rhinorrhea, F, malaise, sneezing)
-paroxysmal stage: 1-6 wks, violent spasmodic productive cough (whoop – narrow glottis with thick sputum), V usually follows cough
-convalescence stage: 2-3 wks, cough for months after inf gone

Front 88

Bordetella Pertussis
Epidimiology

Back 88

-humans sole reservoir
-usually a childhood disease
-targets mucous membranes
-transmission by direct contact or inhaling droplets
*can also be by contaminated objects

-immunization programs have affected incidence A.W.A. carriage in those immune

Front 89

Bordetella Pertussis
Diagnosis

Back 89

-isolation during catarrhal stage
-streak plate with nasopharyngeal swab passed through penicillin or cephalosporin
-BCH ID and use PCR

Front 90

Bordetella Pertussis
Treatment/Contol

Back 90

-immune human globin early in disease for infants < 2yrs
-supportive (suction for secretions, hydration)

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Front 112

Francisella Tularensis
General Info

Back 112

-causes tularemia = rabbit fever, tick fever, deer fly fever, and glandular fever
->G- coccobacillus
-very small

Front 113

Francisella Tularensis
Pathogenesis

Back 113

-intracellular parasite – survives a long time in Macrophages-inhibits phagosome/lysosome function

Front 114

Francisella Tularensis
Clinical Manifestation

Back 114

-after 3 days: fever, chills, malaise, and fatigue
-presents as:
1.Ulceroglandular – most common (necrotic center with raised borders, localized lymphadenopathy)
2.Oculoglandular-results in conjuctivitis and regional lymphdenopathy
3. Glandular
4. Typhoidal
5. Gastrointestinal
6. Pneumonic

Front 115

Francisella Tularensis
Epidimiology

Back 115

-reservoirs: rabbits, ticks, muskrats
-transmission through insect bite or contact with the animal or animal w/ previous contact
-also possible through consumption of cont. meat or water or inhalation of aerosols
-low infectious dose
-incidence low overall w/ cases in AK, MI, OK

Front 116

Francisella Tularensis
Diagnosis

Back 116

-specimen processing hazardous
-lab acquired infections are common

Front 117

Moraxella
General Info

Back 117

- G- bacilli
-M. Catarrhalis
-part of normal flora of the upper respiratory tract

Front 118

Moraxella
Clinical Manifestations

Back 118

-significant agent of otitis media in children
-other infections: bronchitis, sinusitis, and bronchopneumonia

Front 119

Moraxella
Epidimiology

Back 119

-normal flora of URT

Front 120

Acinetobacter
General Info

Back 120

- G- bacilli
-occurs as an opportunistic pathogen

Front 121

Acinetobacter
Epidimiology

Back 121

-primarily in comprimised pts.
-common cause of nosocomial respiratory infections
-likes moist environments
-contaminants of respiratory equipment

Front 122

Escherichia Coli
General Info

Back 122

1) G-, short rod
2)Facultative anaerobic member of Enterobacteriaceae family

-has O, H, K antigens
-5 virotypes based on virulence factors
-O Ag = serogroup
-H Ag = serotype

Front 123

Escherichia Coli
Pathogenesis/ Clinical Manifestations

Back 123

-ETEC  SI, traveler’s D
-EAggEC  SI, persistent infant D
-EPEC  SI, epidemic infantile D (non-bloody stools)
-EIEC  LI, watery D (dysentery, scant bloody stools w/ mucus)
-EHEC  LI
• Verocytoxins SLT-1 & SLT-2
• Mild to moderate D, hemorrhagic colitis, hemolytic uremia syndrome (HUS)
• From foods of animal origin (meat & unpasteurized milk)
• @ any age group

Front 124

Escherichia Coli
Epidimeology

Back 124

-not person to person, but contaminated food

-traveler’s disease
-occurs in everyone & nosocomial infants
-common source if outbreaks
-O, H & K are associated w/
> virulence

Front 125

Escherichia Coli
Diagnosis

Back 125

-assay by nucleic acid probe for enterotoxins or presence of toxin genes on plasmids (more common)
-serology for epidemiology

Front 126

Neisseria Meningitidis
Treatment/Control

Back 126

1) meniingitis and meningoccemia- Ceftriaxone

2)Polyvalent capsular vaccine
-> people older than 65 and international travelers
3)Conjugate vaccine (Menactra)

Front 127

Neisseria Meningitidis
General Info

Back 127

1)G- cocci in pairs with adjacent sides flattened, no flagella, pili, capsule and fibriae
-facultative anaerobes
kidney shaped
-fastidious
-susceptible to adverse conditions(sunlight, cold, hot)
-enhanced growth with CO2 conc.
-Thayer-MArtin medium
-capsular polsacc form 12 serotypes
-A, B, C, Y and W135 cause meningococcal disease

Front 128

Neisseria Meningitidis
Pathogenesis

Back 128

-enter via URT using fimbriae for colonization
-spreads to skin, meninges, joints, eyes, lungs
-capsules inhibit phagocytosis and cause sytemic infections in those w/o capsular or noncapsular Abs
-LPS-highly toxic-> causes vascular damage and circulatory collapse

Front 129

Neisseria Meningitidis
Clinical Manifestations

Back 129

-mild febrile disease w/ or w/o pharyngitis
-pneumonia
-fulminating meningococcemia
-meningitis

Front 130

Neisseria Meningitidis
Epidimiology

Back 130

-droplet infection w/ close contact
-usually in closed populations
-adult carrier lasts days-months
-M/M highest in kids 4-12 months
-B most common type in US
-3rd most common cause of meningitis
-1st among people 5-29 yrs

Front 131

Neisseria Meningitidis
Diagnosis

Back 131

-blood, CSF (best), skin lesions
-(+) nose culture only means carrier state
-thayer-martin medium (Increase CO2)
-isolation of oxidase-positive, gram-negative diplococci, grown on chocolate blood agar->for preliminary ID
-distinguish from Nesseria gonorrhoeae
-LA, CIE, or slide agg. for serotyping

Front 132

Neisseria Gonorrhoeae
General Info

Back 132

1)G- cocci in pairs with adjacent sides flattened, no flagella, pili, capsule and fibriae
-facultative anaerobes
kidney shaped
-fastidious
-susceptible to adverse conditions(sunlight, cold, hot)
-enhanced growth with CO2 conc.
-Thayer-MArtin medium

Front 133

Neisseria Gonorrhoeae
Pathognesis

Back 133

-infection during sexual activity
-1 infection site: men  urethra & women  urethra, cervix
-also possible in the pharynx, anorectal region or conjunctiva
-anchor to surface urethral cells with fimbriae
-possible infection of PMNs  systemic spread
-virulence factors: fimbriae (adherence & promotion of Endocytosis) and LOS (inflammatory response)
-phase variation and lack of immunity grt repeat infections due to differences in pilin, Opa, & LOS

Front 134

Neisseria Gonorrhoeae
Clinical Manifestations

Back 134

MALES
-22% chance of getting bacteria from intercourse
-incubation is 2-8 days
-symptomatic and abrupt with burning urination and yellow, purulent urethral discharge – maybe a fever
-asymptomatic in 10% of cases
-complications (1%) include urethral strictures, epididymitis, and prostatitis
FEMALES
-risk of acquisition higher with 20-80% asymptomatic
-burning or frequency of urination, vaginal discharge, fever, abd pain
-spreads externally to the rectum
-major complications are salpingitis & PID
-other primary inf sites in M&F are rectum, pharynx, & conjunctiva
DISSEMINATED GONOCOCCAL DISEASE
-1-3% of females and much lower % in men
-arthritis-dermatitis syndrome
-asymptomatic genitourinary infection with fever, chills, malaise, arthritis, and skin lesions (wrists, elbows, and ankles)
POSSIBILTY OF INFECTION IN CHILDREN
-infection through birth canal (opthalmia neonatorum = purulent conjunctivitis)
-infection of any mucous membrane can occur

Front 135

Neisseria Gonorrhoeae
Epidimeology

Back 135

-2nd most common cause of venereal disease in the US
-one of the most frequently reported disease in US
-venereal transmission
humans only reservoir
-1 reservoirs are asymptomatic people who are chronic carriers
-highest rates occur in 15-30 (those w/ > sexual activity)
-Host Factors: number of sex partners and contraceptive practices

Front 136

Neisseria Gonorrhoeae
Dianosis

Back 136

-gram stain showing PMNs w/ intracellular G- diplococci (not for females)
-Thayer-martin (CO2)
-nucleic acid amplification assays
-confirm w/ DFA (asymp. F)
-ELISA using urethral pus or cervical swabs (accuracy vary)
-genetic probes

Front 137

Neisseria Gonorrhoeae
Treatment/Control

Back 137

-look @ CDC reccom.
-resistance to penicilin G and tetracycline and flouroquinolines common
-infection of cervix, urethra,rectum- cefixime + (anti-chlamydial) azithromyocin or doxycycline or ceftriaxone + antichlamydial

-ceftriaxone, cefotaxime, or spectinomycin w/ tetracycline
-report cases and advise patients about sex partners

Front 138

Salmonella
General Info

Back 138

-Gram neg. bacilli w/ flagilla

-S. Enterica (2300 serotypes)
-4 total subspecies cause human disease
1. S. Typhi
2. S. Enteritis
3. S. Typhimurium
4. S. Cholerasuis
-3 major Ags (H, O, K)
-G-, nonsporeforming
-produce H2S & gas (glucose fermentation)
-bile resistant

Front 139

Salmonella
Pathogenesis

Back 139

ability to grow withion M cells of peyers patches nad nonactivate macrophages

Front 140

Salmonella
Clinical Manifestations

Back 140

-SALMONELLOSIS
(s.enteritidis) ENTERITIS & DIARRHEA
-ingestion of organisms
-colonization of the LI
-mucosal invader
-acute inflamm & ulceration
-activation of AC
-fluid release  D
-SEPTICEMIA (s.cholerasuis and s.typhi)
-F, chills, anorexia, & anemia
-focal lesions can develop in any tissue
-gastroenteritis is minor or absent
-bacteria rarely isolated from feces
-TYPHOID FEVER(s. typhi)
-1st wk: F, lethargy, malaise, & C (bacteria inf intestinal walls)
-2nd wk: prolonged bacteremia after intracellular replication
-inf of biliary system & acute febrile illness lasting 3-5 wks
-Signs: F of 104, tender abd w/ perhaps rose-colored spots, as bacteria re-infect the intestinal tract from the gallbladder  D
-Complications: intestinal perforation, bleeding & pneumonia

Front 141

Salmonella
Epidimiology

Back 141

Salmonellosis
-one of most common bacteria in US, under-reported
-transmission: food and water
-large animal reservoir (Beef & chicken) but also humans
-large amount needed to infect
Typhoid Fever
-human carriers only (gallbladder)
-spread by fecal water
-carrier state lasts wks-yrs
-acquired during travel to endemic areas & problem in developing countries

Front 142

Salmonella
Diagnosis

Back 142

-gastroenteritis: isolation from feces, BCH ID, serological tests for the O Ag
-septicemia and typhoid fever: blood cultures in 1st two weeks, BCH ID to determine the Vi Ag (K Ag)

Front 143

Salmonella
Treatment/ Control

Back 143

Gastroenteritis:
-replace fluids
-control pain, N & V
-DO NOT USE antibiotics b/c prolong carrier state but recommended for Tx of septicemia and typhoid fever
-vaccines for TF effective
-control by reducing water and food contamination
-reportable diseases-salmonella and tf

Front 144

Shigella
General Info

Back 144

-G-, nonmotile (no flagella)
-facultative anaerobic
-no H2S & no gas
-bile inhibits it
-S. Dysenteriae
-S. Flexneri
-S. Sonnei

Front 145

Shigella
Pathogenesis

Back 145

-virulence factors: endotoxin, enterotoxin (shiga toxin) w/ cytotoxic and neurotoxic activity
-adheres well to intestinal colonic epithelial cells (due to LPS)
-lesions in intestinal tract allow bacteria to penetrate and cause cell death
-induces endocytosis to grow in cell to allow shiga toxin to kill
-4 day incubation period
-mild-inflammation, micro-ulcers and gross ulcers

Front 146

Shigella
Clinical Manifestations

Back 146

Shigellosis:
-asymptomatic to severe bacillary dysentery with fever, chills, severe D, abd cramps, blood and pus in stools, and convulsion
-runs course in 10 days

Front 147

Shigella
Epidimiology

Back 147

-high mortality among infants and debilitated
-humans are natural hosts
-fecal oral route or mechanical vectors (5 F’s)
-low infective dose (< 200 org)
-carrier for 1-4 weeks
-majority cases in US in kids 1-10 yrs old
-S. Sonnei is most common

Front 148

Shigella
Diagnosis

Back 148

-DDx: loose stool w/ mucus w/ bright red blood w/ no N/V
-fresh passed specimens so acids won’t inhibit growth
-BCH Tests (triple-sugar-iron agar)
-Serological tests

Front 149

Shigella
Treatment/Control

Back 149

-treat dehydration and fever
-treat infections with antibiotics
-safe water supply, sewage treatment, handwashing
-reportable disease

Front 150

Yersinia Enterocolitica
General Info

Back 150

-G-, enveloped coccobacilli w/ bipolar staining
-causes severe gastrointestinal infections (enterocolitis)

Front 151

Yersinia Enterocolitica
Pathogenesis

Back 151

> metabolic activity @ 22-25 degrees C

Front 152

Yersinia Enterocolitica
Clinical Manifestation

Back 152

-primarily in colder areas of North America (22-25 deg. C)
-water, milk, wild and domestic animals
-milk and contaminated meat linked to epidemics

Front 153

Yersinia Pestis
General Info

Back 153

-G-, enveloped coccobacilli w/ bipolar staining
-causes bubonic and pneumonic plague

Front 154

Yersinia Pestis
Pathogenesis

Back 154

-protein polysaccharide capsule is antiphagocytic
-heat-labile exotoxin (murine toxin) acts on mitochondria
-Pimary lesion and infection @ site of flea bite

Front 155

Yersinia Pestis
Clinical Manifestations

Back 155

BUBONIC PLAGUE
-sudden onset w/ low fever, prostration, slurred speech, & abd pain
-regional lymph nodes
->infected & inflamed (bubo that is firm and moveable)
-bacteremia spreads to spleen, meninges, skin or lungs
-septicemia -> hemoconcentration, circulatory failure & death
PNEUMONIC PLAGUE
-rapid spread and near 100% MR
-contracted from pts with pneumonic complications
-generalized pain, headache, N, respiratory difficulty, F, cough w/ blood tinged sputum, -> cyanosis and death from suffocation

Front 156

Yersinia Pestis
Epidimiology

Back 156

Sylvatic Plague
-wild rats and other rodents
-to humans by fleas
-fleas infected from rodent blood meal
-western US -> rats, squirrels, and prairie dogs
-also by ingestion or handling
Pneumonic Plague
- > potential for rapid trans.
-person to person
-isolate pts

Front 157

Yersinia Pestis
Diagnosis

Back 157

-blood, sputum, lymph node biopsy
-clinical specimens hazardous
-FA, guinea pig inoculation
-send to appropriate lab for ID

Front 158

Yersinia Pestis
Treatment/Control

Back 158

-antibiotic (streptomycin) therapy w/in 12-15 hours after appearance of fever
-vaccine available for researchers and travelers
-quarantinable disease

Front 159

Vibrio Cholerae
General Info

Back 159

-G- straight or curved rods (comma-shaped)
-monotrichous or lophotrichous flagella
-Na ions increase growth rate
-O Ag for grouping

Front 160

Vibrio Cholerae
Pathogenesis

Back 160

-virulence factors: enterotoxin, flagellum, & fimbriae
-cholera toxin (A-B type)-> causes cAMP levels to rise->disrupts function of ion pumps, creating an ion imbalance that leads to diarrhea

Front 161

Vibrio Cholerae
Clinical Manifestation

Back 161

-abrupt onset of V/D w/ incubation period of a few hours
-fluid loss 15-20 L/day
-voided fluid is watery w/ flecks of mucus, w/o odor (rice water diarrhea)

Front 162

Vibrio Cholerae
Epidimiology

Back 162

-widespread epidemics
-Primary route is fecal-oral
-fresh water or salt water
-human carriers as reservoirs, convalescent carriers shed for months after illness
-chronic carriers shed intermittently for yrs (from gallbladder)
-theory: permanent reservoir in selected marshes & estuaries of subtropical & tropical areas
-US -> sporadic cases in gulf coast states involving seafood

Front 163

Vibrio Cholerae
Treatment/Control

Back 163

-replacement of fluid and electrolytes
-initial shock w/ IV fluids
-vaccination good in 50% pts but no long lasting immunity
-used for travelers (not recc)
-reportable disease

Front 164

Vibrio Vulnificus
General Info

Back 164

-G- straight or curved rods (comma-shaped)
-monotrichous or lophotrichous flagella
-Na ions increase growth rate
-O Ag for grouping

Front 165

Vibrio Vulnificus
Clinical Manifestations

Back 165

-wound infections and septicemia
-mild infection to severe cellulitis
-bullous skin lesions

Front 166

Vibrio Vulnificus
Epidimiology

Back 166

-fresh water or salt water (estuaries or coastal waters)
-occurs after ingestion of raw or poorly cooked seafood
-MR as high as 20-50%

Front 167

Campylobacter Jejuni
General Info

Back 167

- G-
-vibrio-like, comma-shaped, spiral or s-shaped
-pairs look like wing of a seagull
-Most common cause of bacterial gastroenteritis in the U.S.
-LPS
-enterotoxin
-flagella

Front 168

Campylobacter Jejuni
Clinical Manifestations

Back 168

-acute gastroenteritis, fever, D (liquid, blood or both), abd pain
-older, compromised people it appears as acute febrile bacteremia with inflammatory bowel disease and cause death

Front 169

Campylobacter Jejuni
Epidimeology

Back 169

-normal flora of mammals and birds
-contaminated water, milk, chicken, and other foods
-one of the leading causes of bacterial diarrhea worldwide
-people who lack gastric acids @ risk
-person to person and fecal-oral

Front 170

Campylobacter Jejuni
Diagnosis

Back 170

-isolation and ID w/ BCH
-specialized media
-> Campy BAP
-Decrease [O2] @ 42 degrees C
*slow growers (48-72 hrs)

Front 171

Helicobacter Pylori
General Info

Back 171

G- spiral shaped or gull-winged with 6 polar sheathed flagella

Front 172

Helicobacter Pylori
Pathogenesis

Back 172

-increased by motility, urease, adhesins, LPS, and vacuolating cytotoxin & cagA
-resides in the stomach or occasionally the esophagus

Front 173

Helicobacter Pylori
Clinical Manifestations

Back 173

-gastritis and development of gastric or peptic ulcers
-gastric adenocarcinoma
-b cell lymphomas

Front 174

Helicobacter Pylori
Epidimiology

Back 174

-Humans are primary resorvoir
-person-person trans. (fecal-oral)
-worldwide incidence is high
-1/2 of adults are carriers
-in 70-100% of patients with gastritis, gastric ulcers, and duodenal ulcers

Front 175

Helicobacter Pylori
Diagnosis

Back 175

-ELIZA for IgG or IgA in saliva or plasma
-gastric biopsy, isolation and cultivation, urease test
-urea breath test (oral 14C)
-PCR

Front 176

Helicobacter Pylori
Treatment/Control

Back 176

-2 or 3 antimicrobials (amoxicillin plus metronidazole or bismuth subsalicylate)
-1 antib + antisecretory agent (histrionic H2 antagonist) has had poor results

Front 177

Brucella
General Info

Back 177

-causes Brucellosis = undulant fever = malta fever, Bangs Disease (cattle)
-B. Melitensis
-> G- ; coccobacilli

Front 178

Brucella
Pathogenesis

Back 178

-multiply in PMN’s and M
-lesions consist of small granulomas made up of epitheloid cells, PMNs and lymphocytes
-incubation is days to months, onset varies
-relapses are hallmark of the disease

Front 179

Brucella
Clinical Manifestation

Back 179

-fatigue is the most common complaint
-other Sx: diurnal fever, anorexia, muscle aches, headaches, backaches
-chronic Sx: weakness, fatigue, vague pains, & depression ->, lasting 1-20 years

Front 180

Brucella
Epidimiology

Back 180

-related to animal infections
-ingestion, contact and inhalation (US usually contact)
-human US inf -> cattle & hogs
-occupational hazard
-consumption of unpasteurized milk or dairy products

Front 181

Brucella
Diagnosis

Back 181

-fever of unknown origin
-isolation from blood, BM, or liver
-serological test can indicate active disease
-Primary culture should be incubated for 4-6 weeks (b/c of intracellular position) or will be a negative result

Front 182

Brucella
Treatment/Control

Back 182

-vaccine for animals
->eliminates human disease

Front 183

Pseudomonas
General Info

Back 183

- G- rods, single polar flagellum, capsule-like envelope or slime layer and NO spores
-P. Aeruginosa
-can resist harsh situations and survives well in water

Front 184

Pseudomonas
Pathogenisis

Back 184

-biofilm development
-alginate synthesis
-LPS
-antibiotic resistance

Front 185

Pseudomonas
Clinical Manifestation

Back 185

-any tissue can be infected (not usually mucosa though)
-opportunist that is common in hospitalized patients
-common in pts with CF, burns, leukemia, UTI in catheters of pts w/ spinal cord injuries, and swimmer’s ear in diabetics
-also: folliculitis, keratitis, endopthalmitis (contaminated eye soln), ecthyma gangrenosum (black ulcers) w/ direct invasion of BV

Front 186

Pseudomonas
Epidimiology

Back 186

-present everywhere
-common in hospitals
-pt to pt transmission
-food and water contamination

Front 187

Pseudomonas
Diagnosis

Back 187

-various testing after isolation
-blue-green pigment, grape-like odor

Front 188

Pseudomonas
Treatment/Control

Back 188

-gains resistance during therapy
-pooled human immune globin with antibiotics
-hospital prevention techniques for control
-In addition to antibiotics use mucolytic agents, chest PT, and postural drainage in pts. with chronic lung disease (CF)

Front 189

Stentrophomonas Maltophilia
General Info

Back 189

-looks like pseudomonas
- non-sporulating G- bacilli w/ polar flagella

Front 190

Stentrophomonas Maltophilia
Pathogenesis

Back 190

-affected by ability to adhere to plastic, glass and Teflon and to survive and multiply in various types of IV insulfates

Front 191

Stentrophomonas Maltophilia
Clinical Manifestations

Back 191

-bacteremia, endocarditis, RT infection, CNS infection, opthalmologic, UTI, skin and soft tissue infection, bone and joint infection, and GI infection

Front 192

Stentrophomonas Maltophilia
Epidimiology

Back 192

-isolated from nosocomial sources (blood tubes, dispensers, dialysis, disinfectant, shower heads, faucets, personnel’s hands)
-human carriage ???

Front 193

Stentrophomonas Maltophilia
Treatment/Control

Back 193

-resistance is a problem with antibiotics
-penicillins and cephalosporins are ineffective

Front 194

Legionella Pneumophilia
General Info

Back 194

- G- bacilli, poorly staining
-obligate aerobes
-req. charcoal yeast medium
-slow growers
-primary human pathogen

Front 195

Legionella Pneumophilia
Pathogenesis

Back 195

-facultative intracellular parasites in Macrophages
-prevents lysosome-phagosome function
-survives in biofilms and protozoans

Front 196

Legionella Pneumophilia
Clinical Manifestations

Back 196

-headache, malaise, myalgia and dramatic temp Increased w/in 24 hrs
-non-productive cough, and maybe systemic stuff (V, D, abd pain)
-later: bronchopneumonia, XR for patchy regions (fluid)
-death preceeded by impaired renal fxn, shock and/or resp. failure
-Pontiac Fever
-less severe illness w/ a short incubation time
-F, headache, myalgia, dry cough NO PNEUMONIA

Front 197

Legionella Pneumophilia
Epidimiology

Back 197

-smokers and IMCD are @ risk
-many cases in persons > 50
-airborne transmission
-hospitals major source of infections
-NO person to person trans.
-central air conditioning systems and water systems in hospitals

Front 198

Legionella Pneumophilia
Diagnosis

Back 198

-DFA, take aspirate and test
ELISA, RIA, indirect FA
-difficult to send specimens to lab (infectious)

Front 199

Legionella Pneumophilia
Treatment/Control

Back 199

-erythromycin or rifampin
-maybe O2 therapy, nasoactive drugs and/or renal dialysis
-control by cleaning air conditioning systems
-hyperchlorinate water

Front 200

Treponema pallidum
General Info

Back 200

-G- spirochete w/ 3 periplasmic flagella, helically coiled, long, corkscrew shaped
-T. Pallidum major pathogen
-cannot be grown on lab media, needs rabbit epithelial cells @ low O2 or on rabbit testicles
-microaerophile
-extremely sensitive to heat, drying osmotic stress, & aerobic conditions

Front 201

Treponema pallidum
Pathogenesis

Back 201

-surface mucoid coat (impedes Ag access)-act as adhesions
-invasion of MM or abrasions & dissem. to blood via lymph
-incubation period 10-90 days
-female Primary lesion -> labia, vaginal wall or cervix
-male Primary lesion -> shaft of the glans of the penis
-both -> lips, tongue, tonsils, & anus

Front 202

Treponema pallidum
Clinical Manifestations

Back 202

SYPHILIS
-Primary disease:
-papule develops w/ superficial ulcer (hard chancre)
-painless lymph node enlargement
-40-60% pts pass through Primary & Scondary ds w/o knowing they have it
-Secondary disease:
-inflam of skin, MM & CNS in 2-12 wks after the Primary lesion
-F, sore throat, general lymphadenopathy, headache, rash (palms
& soles)
-Tertiary disease:
-gummas
-most destructive due to enhanced immunological host rxn in skin
& bones
-neurosyphilis – syphilitic meningitis or tabes dorsalis,
complications -> paralytic dementia & ALS
-80% fataliites
-Congenital disease
-from transplacental infectionand 50% are stillborn or abort
-Hutchinson’s Triad -> interstitial keratitis, notched incisors
& 8th N deafness

Front 203

Treponema pallidum
Epidimiology

Back 203

-vigorous immune response but ds not usually eradicated -> persistent infection
-dense coat protects against specific Ab attachment
-UnTx persons are fairly resistant to re-infection
-people Tx during early Secondary or Primary stages are fairly susceptible to re-infection

-Humans are the only natural host
-not highly contagious disease
-sexual transmission most common route
-only Primary or Secondary are contagious
-most frequent in sexually active (15-30)

Front 204

Treponema pallidum
Diagnosis

Back 204

-cannot be cultured in vitro
-direct microscopic observation using darkfield microscopy
-serological tests using Wassermann Abs specific for cardiolipin
-FTA-Abs
-Two most common tests: VDRL, and RPR

Front 205

Treponema pallidum
Treatment/Control

Back 205

PENICILLIN
7-10 days for the Primary ds
2 & 3 -> prolonged Tx
-Congenital and late syphilis- penicillin G
-Tetracycline and doxycycline can be used if allergic to penicillin
-a reportable disease
*Jarisch Herxheime
r Reaction may follow Tx of 2 & 3 ds

Front 206

Borrelia
General Info

Back 206

1)G- spirochete
-B. Burgdorferi* (Lyme Ds) & B. Recurrentis** (relapsing fever)

* = minor Ag shifts
** = major Ag shifts

Front 207

Borrelia
Clinical Manifestations

Back 207

Lyme Disease
-Stage 1: erythema migrans, perhaps fever, minor problems (lymphad)
-Stage 2: disseminated infection, severe fatigue, lesions, joint & muscle pain
-Stage 3: persistent infection, longer episodes of arthritis & chronic episodes of arthritis, bluish-red swollen skin lesions, encephalomyelitis or keratitis
-Congenital Infection: transplacental inf, reported in infants contracted the disease in 1st trimester
Relapsing/Tick/Recurrent Fever
-abrupt onset, no toxins, chills, fever, severe headache, muscular/joint pains, enlargement/tenderness of the spleen and liver
•Epidemis borreliosis-Louse borne – SEVERE, single relapse
•Endemic borreliosis-Tick borne – several relapses, less severe

Front 208

Borrelia
Epidimiology

Back 208

-most common insect vector borne inf in the US
-life cycle involves ticks and mice
-preferred hosts for adult ticks are white-tailed deer
-Lyme ds does occur in some domestic animals (dogs, horses, cattle)
-Epidemic Borreliosis -> imported from human louse
-Endemic Borreliosis - tick vectors & animal reservoir (W & SW US)

Front 209

Borrelia
Diagnosis

Back 209

-IFA is the best test
-also ELISA and PCR
-demonstration of bacteria in blood

Front 210

Borrelia
Treatment/Control

Back 210

Tetracycline

Front 211

Leptospira interrogans
General Info

Back 211

-Weil’s Disease AKA leptospirosis
-G- helical spirochetes w/ hooked ends
-multilayered outer envelope

Front 212

Leptospira interrogans
Pathogenesis

Back 212

-no toxins
-invasion is via mucosa & broken skin
-no lesion at the site of entry

Front 213

Leptospira interrogans
Clinical Manifestations

Back 213

-eliminated in most areas except for the kidneys (mild, transient proteinuria to severe nephritis w/ decreased or no urine output)
-interstitial nephritis with glomerular swelling
-severe headache, chills, and fever with relapses
-Jaundice in severe cases and kidney failure is the most common cause of death

Front 214

Leptospira interrogans
Epidimiology

Back 214

-zoonotic ds (rodents)
-in US the major source of human infection is dogs, rats and farm animals
-bacteria in urine -> to humans via infected soil, water and food
-survives for months in wet soils or water

Front 215

Rickettsia
General Info

Back 215

-G- coccobacilli
-obligate intracellular parasites w/ long generation time

Front 216

Rickettsia
Pathogenesis

Back 216

-Induce phagocytosis and enter endothelial cells
-replicate in cytoplasm or nucleus of host cells

Front 217

Rickettsia
Clinical Manifestations

Back 217

-Induce phagocytosis and enter endothelial cells
-replicate in cytoplasm or nucleus of host cells
CLASSIC TRIAD OF DISEASES -> Fever, headache & rash

Front 218

R. Rickettsii
General Info

Back 218

Etiologic agent of rocky mountain spotted fever (RMSF)

Front 219

R. Rickettsii
Pathogenesis

Back 219

-widespread endothelial damage w/ occlusion of small vessels, microhemorrhages, electrolyte changes and perhaps necrosis, shock and death

Front 220

R. Rickettsii
Clinical Manifestation

Back 220

-incubation is 3-12 days, onset is sudden w/ severe headache, fever, malaise & myalgia
-2-4 days after onset -> rash appears on palms/soles
-other Sx: GI complaints, conjunctivitis, and stiff neck

Front 221

R. Rickettsii
Epidimiology

Back 221

-transmission by ticks as reservoirs and vectors
-from inf hosts or transovarial
-RMSF -> most severe and common rickettsiosis in US
-N & S Carolina, OK
-most often in kids & young adults

Front 222

R. Rickettsii
Diagnosis

Back 222

-biopsy skin lesion and use microscopy using DFA
-indirect FA or LA
-Weil-Felix Test: Ab to proteus sp. and is not used anymore
-isolation not recommended -> difficult and requires special facilities

Front 223

R. Rickettsii
Treatment/Control

Back 223

Antibiotic treatment Should begin immediately

Front 224

R. Prowazekii

Back 224

Causes epidemic typhus

Front 225

R. Typhi

Back 225

Causes murine typhus

Front 226

Coxiella burnetii
General Info

Back 226

1) G-, obligate intracellular bacterium
-Etiologic agent of Q fever
-highly resistant to heat, cold, sunlight, drying, & chemicals (unique)

Front 227

Coxiella burnetii
Clinical Manifestations

Back 227

-subclinical to flu-like to pneumonia w/ prolonged fever & possibly hepatitis
-NO RASH
-Most common presentation: subacute endocarditis->occurs on prosthetic or previously damaged heart valve

Front 228

Coxiella burnetii
Epidimiology

Back 228

-US outbreaks with livestock, livestock products or lab inf
-arthropod-vertebrate-arthropod cycle
-major reservoirs: cattle, sheep, & goats (NOT humans)
-inhalation of dust particles & aerosols
-ingestion & handling of infected meat & milk

Front 229

Ehrlichia chaffensis
General Info

Back 229

Etiologic agent of human monocytic Ehrlichiosis

-obligate intracellular bacteria

Front 230

Ehrlichia chaffensis
Clinical Manifestations

Back 230

-fever, headache, malaise, & myalgia
-rash in 30-40%
-leukopenia andthrombocytopenia occur

Front 231

Ehrlichia chaffensis
Epidimiology

Back 231

Transmission via ticks

Front 232

Bartonella Henselae
General Info

Back 232

G- bacilli
-Causes cat scratch disease

Front 233

Bartonella Henselae
Clinical Manifestations

Back 233

-Bacillary angiomatosis
-Cat Scratch Fever- fever, lymphadenopathy, & osteolytic lesions
-Subacute endocarditis

Front 234

Bartonella Quintana
Epidimeology

Back 234

-AIDS pts

Front 235

Bartonella Henselae
Treatment/Control

Back 235

antibiotics

Front 236

Chlamydiae
General Info

Back 236

-very small G- nonmotile cooci
-no peptidoglycan
-obligate intracellular parasite
-inclusion bodies (cannot be seen with LM)
-LPS but little
-very small genome
-unable to synthesize ATP

Front 237

C. Trachomatis
Clinical Manifestations

Back 237

TRACHOMA
-infects conjunctival epithelial cells -> development of follicles w/ inclusion bodies
-cornea -> vascularized and clouded
-eyelids -> scarred & malformed causing trichiasis (inward eyelids)
-continued cornea scratching leads to opacification
INCLUSION CONJUNCTIVITIS (IC)
-milder than Trachoma
-self-limiting purulent conjunctivitis
-keratitis and corneal infiltrates
-scarring may occur w/ chronic infection
NONGONOCOCCAL GENITAL/RECTAL INFECTIONS
-dual infection with gonorrhea
-men ->most sympt. are symptomatic-> urethritis, epididymitis, proctitis
-women -> most smpt. are asymptomatic->mucopurulent cervicitis, endometritis, urethritis,salpangitis, PID, perihepatitis
-INFANTS => nasopharyngeal infection occurs during passage through cervix
-Reiter’s Syndrome -> urethritis, conjunctivitis, polyartritis
LYMPHOGRANULOMA VENEREUM (LGV)
-inguinal lymphadenopathy
-initial lesions/vesicles appear on male/female urogenital tract
-Infant pnemonia
-Neonatal conjuctivitis

Front 238

C. Trachomatis
Epidimiology

Back 238

TRACHOMA
-hot & dry area
-spread by flies, fingers and dirty towels
-initial infection during childhood
IC
-most common form of neonatal conjunctivitis in US
-autoinoculation and oral-genital contact
-adult inf from swimming pools
NONGONOCOCCAL G/R INF
-most common bac STD in US
-highest in 15-24 yr olds
-recent decline
-50-70% of women clinically silent
-40%W & 20%M with gonorrhea have chlamydia
-1/3 of infant interstitial pneumonia
-mc -> young adult white males
LGV
-sexual intercourse
-lower socioeconomic groups
-Male homosexuals major resoirvoir in US

-20:1 male to female ratio

Front 239

C. Trachomatis
Diagnosis

Back 239

NONGON G/R INF
-DFA
-EIA
-NA probe
-PCR
-culture for inclusion bodies
LGV
-clinical picture
-isolation from aspirated bubos
-others same as NGU
-Frei test = intradermal test no longer used

Front 240

C. Trachomatis
Treament/Control

Back 240

NONGON G/R INF
-azithromycin
-doxycycline
-erythromycin
-ofloxicin
-Tx for gonorrhea as well
LGV
-azithromycin
-doxycycline

Front 241

C. Psittaci
General Info

Back 241

-causes psittacosis or ornithosis

Front 242

C. Psittaci
Epidimiology

Back 242

-rare in the US
-psittacosis from psittacine birds
-ornithosis from other birds
-resp tract is the main site of entry through bird droppings
-P->P also

Front 243

C. Pneumoniae
Clinical Manifestations

Back 243

-acute RT infections  sinusitis & bronchitis (walking pneumonia)

Front 244

C. Pneumoniae
Epidimiology

Back 244

-6-20% of community acquired pneumonia infections
-correlation w/ atherosclerosis -> bacteria in fatty streaks and plaques
-P->P transmission by respiratory droplet
-outbreaks in families, schools, military barracks, and nursing homes
-coinfection w/ viruses
-reinfections are common

Front 245

C. Pneumoniae
Diagnosis

Back 245

-NAAT's
-EIA, DFA for Ag, PCR
-microimmunoflourescence for serology

Front 246

Mycoplasmas & Ureaplasmas
General Info

Back 246

-smallest and simplest of bacteria
-lowest G+ C values
-lack a true cell wall
-triple layered membrane
-colonies are fried egg shape
-M.pneumoniae(upper and lower Resp. Tract Infect); M. hominis(BV); and U.urealyticum(enitourinary tract infections)

Front 247

Mycoplasmas & Ureaplasmas
Pathogenesis

Back 247

M PNEUMONIAE
-no toxins
-adhere specifically to epithelial cells  interfere with ciliary actions -> stimulate an inflamm reaction and exudate

Front 248

Mycoplasmas & Ureaplasmas
Clinical Manifestations

Back 248

-incubation period is 9-21 days
-lack of lobar consolidation
-remittent fever, cough, and headache for weeks
-WBC count elevated & cold agglutining +
-long convalescence lasting 4-6 weeks
Stevens-Johnson Syndrome -> bullous lesions on the skin & MM

M. Hominis -> postpartum fever and BV + PID

U. Urealyticum -> nonchlamydial urethritis in men
-> chorioamnionitis and postpartum fever in women
-M.pneumonia->mycoplasma pnemonia

Front 249

Mycoplasmas & Ureaplasmas
Epidimiology

Back 249

M PNEUMONIAE
-20% of pneumonia cases
-transmission by infectious droplet
-infectious dose is low
-epidemics every 4-6 years
-symptomatic inf in 5-15 yr olds
-33% of all inf in teenagers

U. urealyticum and m.hominis-
-infants, particularly girls get at birth
-acquired primarily through sexual contact
-women are frequently asymptomatic and act as reservoirs

Front 250

Mycoplasmas & Ureaplasmas
Diagnosis

Back 250

-microscopy sucks b/c organisms are too small
-serologic tests: MIF, cold agglutinins test

Front 251

Mycoplasmas & Ureaplasmas
Treatment/Control

Back 251

Doxycycline & erythromycin

Front 252

Staph aureus
General Info

Back 252

Nonmotile G+ cocci arranged in clusters
S. Aureus (coagulase +)
S. Epidermidis (-)
S. Saprophyticus (coag -)
S.Lugdenisis (-)

-in 80% of supprative ds-(pus)
-2nd to E. Coli in nosocomial inf
-catalase + under aerobic cond.
-wide T range (6.5 - 46C)
-protein A & polysaccharide A
commonly resistant to penicillin (B-Lactans)erythromycin, & tetracycline

Front 253

Staph. aureas
Pathogenesis

Back 253

Cytolytic toxins(alpha toxin- lyse RBC's), Enterotoxins- cause food poisoning, Exfoliative Toxins- Cause Scalded Skin Syndrome, TSST-1- causes TSS

Front 254

Staph. aureus
Clinical Manifestations

Back 254

Skin infections – one of the most common bacterial human inf
Respiratory Infections – often as a complication
Osteomyelitis – rare, in children
Metastatic Infections – trauma and debilitating ds dispose
Enterocolitis – overgrowth by drug-resistant enterotoxin strains->inflammation of intestines
Food Poisoning – rapid course, in meats, salads & baked foods
TSS
Coagulase - Infections – opportunistic & nosocomial->catheter and shunt infections
-bacteremia
-septic arthritis

Front 255

Staph aureus
Epidimiology

Back 255

-part of normal flora
-human carriers only source of human infection
-epidemic and endemic ds
-most dangerous carriers->food handlers (hospital personnel dangerous in hospitals)
-direct contact via the hands-MOST IMPT.

-> hospital epidemics usually caused by S. Aureus

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Front 260

Staph aureus
Diagnosis

Back 260

-S. Aureus appears golden yellow in isolation
-Susceptible to lysostaphin
-ubiquitous
-inoculate fluids into broth medium
-S. Aureus/Strep DDx -> catalase test <s.aureus(-);strep.(-)>
-S. Aureus/S. Epidermidis DDx -> coagulase test
-Staphylococcus/Micrococcus DDx -> lysostaphin suscept.
-Detect mac A by PCR and pulsed field electrophoresis

Front 261

Staph aureus
Treatment/Control

Back 261

-det. antibiotic sensitivity
-antibiotic & surgical drainage (possibly)
-penicilinase resistant penicillin, 1st generation cephalosporin or vancomycin
-hospital transmission most serious
-segregate individuals with staph infections
-inf control review in hospitals

Front 262

Streptococcus
General Info

Back 262

Non-pathogens & pathogens of the normal flora of the gut & mouth
S. pyogenes, S. pneumoniae (diplococci + lancet shaped), S. agalactia, & S. mutans (Enterococcus=E. faecalis)
G+ cocci in chains or pairs possessing fibrils
-Facultative anaerobes
-Catalase negative
-alpha, beta or gama hemolysis

Front 263

Streptococcus
Clinical Manifestations

Back 263

-in bloodstream, respiratory tract & skin infections
-post-infection problems w/ rheumatic fever & glomerulonephritis

Front 264

Group A Strep (Streptococcus pyogenes) (GAS)
Pathogenesis

Back 264

-M protein & capsule prevent phagocytosis
-Virulence factors: Capsule, M protein, streptolysin O, streptolysin S, pyrogenic exotoxin, streptokinases
-Adherence to fibronectin coat of epithelial cells by fibrils

Front 265

Group A Strep (Streptococcus Pyrogenes) (GAS)
Clinical Manifesations

Back 265

Pharyngitis (most freq. site)
-1 of most common causes of bacterial sore throat
-most freq in ages 5-15, infants rare
-Tx is very important so no progression to scarlet fever
-sore throat, F, headache, tonsillitis, swollen/tender cervical lymph nodes, beefy red pharynx w/grayish-yellow exudates, abd pain, N & V
Scarlet Fever
-like above but skin rash hallmark of disease
-rash appears on upper chest  trunk neck & extremities (face usually unaffected)
-rash followed by desquamation for several weeks
-strawberry tongue -> raspberry tongue
Strep TSS
-hypotension, renal failure & red rash
Skin Infections
-2nd most common site of strep infection producing either pyoderma & erysipelas

Can spread to any system -> impetigo, otitis media, meningitis
Complications -> rheumatic fever and poststreptococcal acute glomerulonephritis (AGN)
-cellulitis
-necrotizing fascilitis
+Bacterimia

Front 266

Group A Strep (Streptococcus Pyrogenes) (GAS)
Epidimiology

Back 266

-phayngitis (cold weather), + pyoderma, otitis media, and impetigo are most common CM

-transmission is via droplets from respiratory secretions (more common in nasal carriers for moist droplets other than dust particles)

-chronic, asymptomatic anal carriers are also a reservior

-impetigo > during spring and fall through direct contact

Front 267

Group A Strep (Streptococcus Pyrogenes) (GAS)
Diagnosis

Back 267

1.Direct Antigen Detection
-latex agglutination
-EIA
-throat swab on blood agar &/or -FA w/ gram stain
-catalase test and bacitracin sensitivity to R/O staphylococcus infection

Front 268

Group A Strep (Streptococcus Pyrogenes) (GAS)
Treatment/control

Back 268

1.Pharyngitis
-Penicillin or erythromycin

2.Soft tissue, Sepsis- Clindamyacin;debriedment

Rheumatic fever – prolonged bed rest & maybe life-long antibiotic therapy

AGN - supportive, restrict Na to prevent fluid build-up & diuretics

Front 269

Group B Strep (Streptococcus agalactiae) (GBS)
General Info

Back 269

leading cause of neonatal sepsis & meningitis

Front 270

Group B Strep(Streptococcus agalactiae) (GBS)
Clinical Manifestations

Back 270

Neonatal Sepsis and Meningitis:
early onset disease
-@ birth or w/in 7 days of birth from the mother
-most common form (> mortality 75%)
-Risk Factors = prematurity, prolonged rupture of membranes, and OB complications
-POE -> URT
late onset disease
-from 7 days up to 8-12 wks after birth
-from nurseries via infected hands of infected mothers or infants
-POE -> mucosal surfaces

-major CM: meningitis or osteomyelitis both w/ or w/o bacteremia

Front 271

Group B Strep(Streptococcus agalactiae) (GBS)
Epidimeology

Back 271

-normal flora of pharynx, GI tract, & vagina

1-3 neonatal cases per 1000 births

Front 272

Group B Strep(Streptococcus agalactiae) (GBS)
Treatment/Control

Back 272

Ampicillin plus Gentamycin for neonates

Front 273

Viridans Strep
General Info

Back 273

-normal flora of respiratory, GI & genital tract
-most common cause of Subacute Bacterial Endocarditis (SBE)
-S.sanguis most common species causing SBE
-S Mutans -> SBE & role in tooth decay

Front 274

Viridans Strep
Pathogenesis

Back 274

Minor trauma may allow bacteria to invade the bloodstream from the pharyngeal region
Pathogenicity can depend on ability to adhere to teeth & form plaque (S. Mutans)

Front 275

Viridans Strep
Clinical Manifestations

Back 275

Causes SBE, meningitis, sinusitis, intra-abd infections

Front 276

Viridans Strep
Treatment/Control

Back 276

Penicillin + aminoglycoside (streptomycin)

Front 277

Strep Pneumoniae
General Info

Back 277

-Pairs of lancet shaped cells
-NO Lancefield Ags
-serotypes based on capsular Ag
-alpha hemolytic
-87% of pneumococcal disease in the US

Front 278

Strep Pneumoniae
Pathogenesis

Back 278

-Smooth types -> virulent
-Rough types -> non-virulent (can be converted to smooth by transformation)
-rarely a Primary infection
-occurs in compromised respiratory pts
-factors that slow epiglottal reflex (chilling, anesthesia) cause aspiration of bacteria from URT
-predisposing factors: respiratory viral inf, cardiac failure & pulmonary stasis from prolonged bed rest
-infection steps
1.invasion directly through bronchial tree
2.edema in alveoli
3.spread peripleurally via bronchioles
4.fibrin accumulation & infiltration of RBCs
5.neutrophil infiltration, RBC lysis, bacteria phagocytized
-adult -> 1 or more complete lobes
-kids & aged -> more patchy
-virulence factors: capsules & pnemolysin

Front 279

Strep Pneumoniae
Clinical Manifestations

Back 279

pneumonia – chills & F (102-106F), severe pleuritic pain, cough (rusty, mucopurulent sputum), in lower lobes, recovery can be as fast as onset
sinusitis & otitis media – most common in young children
meningitis – follows inf of sinuses, ear, or head trauma

Front 280

Strep Pneumoniae
Epidimiology

Back 280

-leading cause of community aquired bacterial pneumonia

-impotant cause of bacterial meningitis (esp older adults)

-in children & infants  most common bacterial causes of pneumonia, otitis media, & bacteremia

-carried in RT of most healthy people (carriage rates > in preschool children)

-transmission directly proportional to frequency & intimacy of content

> incidence in cooler months

Front 281

Strep Pneumoniae
Diagnosis

Back 281

-Physical
-Xray findings
-FA and LA/CIE (K Ag)
-Sputum gram stain, blood agar & optochin sensitivity also use CSF

-> Quellung Rxn
-Bile solubility test
-DFA

Front 282

Strep Pneumoniae
TReatment/Control

Back 282

-Begin immed after physical, XRay, specimen gram stain
-Pneumonia-Penicillin sensitive- IV Ceftriaxone
-Penicillin resistant- IV levofloxacin
-Meningitis- IV vancomycin or cefotaxime
-Otitis Media-amoxicillin if resistant augmentin
(33% resistant to penicillin)
-UnTx Fatality = 30%
-Tx Fatality = 5%
-polysaccharide vaccine for high risk groups (Pneumovax)
-75% effective in adults
-not for children < 2yrs

*Prevnar for children <2yrs (infants)

Front 283

Enterococcus
General Info

Back 283

Most are E. Faecalis or E. faecium
G + ovoid org. in short chains, pairs or as single cells
-Catalase negative
-used to be group D streptococci
-resistant to antimicrobials (B-Lactams), clindamycin and aminocyclitols -> esp Vancomycin
-important as 2 invasions (nosocomial)

Front 284

Enterococcus
Clinical Manifestation

Back 284

-3rd most common cause of nosocomial infections
- > incidence with > in use of antimicrobials or > invasive device use
-UTI – hospitalized pts
-Endocarditis – elderly men
-Bacteremia – urinary tract often a source
-Neonatal Infections

Front 285

Enterococcus
Epidimiology

Back 285

-may originate from normal flora(large intestine and GU tratct)
-P->P transmission
-outbreaks among hospitalized neonates

Front 286

Enterococcus
Diagnosis

Back 286

Isolation and biochemical ID
 Bile-esculin positive
 growth in 6.5% NaCl
-Test for optochin sensitivity (Enterococcus is resistant)

Front 287

Enterococcus
Treatment/Control

Back 287

Test for antibiotic susceptibility

 Synergistic Tx being used

Antibiotics- Linezolid, and quinupristin/dalfopristin

Front 288

Bacillus
General Info

Back 288

-G+ rods that move by using peritrichous flagella
-Endospore formation

Front 289

B. Anthracis
General Info

Back 289

Causes Anthrax
-facultative anaerobe (12-45C)

Front 290

B. Anthracis
Pathogenesis

Back 290

-extremely resistant to adverse chemical and physical environments
-120C for 15 minutes required to inactivate spores
-spores remain viable for years (inf source for long periods)
-if produces capsule (interferes with phagocytosis) & toxin then considered a fully virulent strain
-humans infected by small abrasions, inhalation & ingestion of infected meat -> bloodstream may be infected by any 3

Front 291

B. Anthracis
Clinical Manifestations

Back 291

-exotoxin causes respiratory failure & anoxia (CNS & edema)
-Cutaneous Anthrax (95% of cases)
-2-5 days post inf a papule appears
-few days later -> vesicle w/ bluish-black fluid
-rupture of vesicle reveals black eschar-> malignant pustule
-Pulmonary Infection (aka=Woolsorter Disease)(most rare)
-GI Infection
-N,V,D -> may be blood loss in stool
Meningitis possible from any of the 3 above situations

Front 292

B. Anthracis
Epidimiology

Back 292

-most common-> cutaneous, industrial anthrax-contact w/ animals in endemic area
-Pulmonary anthrax-bioterrorism
-spontaneous ds in herbivorous animals (ingest spores & enters through mucosa)
-ds duration is a few days long & infected animal asympt until a few hours before death
-sporadic cases in the US but all forms are rare in the US

Front 293

B. Anthracis
Diagnosis

Back 293

-Species from malignant pustule, sputum or blood culture

-For pulmonary confirmed case- Clinical illness plus positive culture or 2 other tests i.e PCR, DFA, and serology

-colonies possess and irregular fringelike edge that resemble hair-like curls

Front 294

B. Anthracis
Treatment/Control

Back 294

1)Ciproflaxin
2)Doxycycline
3) Amoxicillin
-deeply bury carcasses to prevent spread of spores in known or suspected animals
-imported animal products need to be gas sterilized
-vaccine available to control human cases in industrial settings & military situations
-active immunization for herbivorous animals

Front 295

B. Cereus
General Info

Back 295

Causes Food Poisoning

Front 296

B. Cereus
Clinical Manifestations

Back 296

2 forms of food poisoning
-incubation of 2-6 hrs w/ severe N & V -> emetic form
-heat-stable enterotoxin (preformed)
-on contaminated rice
-incubation of 16-18 hrs w/ abd cramps & D (diarrheal form)
-heat-labile enterotoxin (produced in situ)
-on contaminated meat or vegetables
-Fulminate eye infections-most common cause of traumatic eye infections

Front 297

B. Cereus
Epidimiology

Back 297

-most common cause of traumatic eye infections-> from soil contamination of object penetrating eye or direct inoculation

Front 298

B. Cereus
Diagnosis

Back 298

-clinical picture, gram stain, & biochemical ID
-food poisoning might involve isolation in food or
-detection of enterotoxin

Front 299

B. Cereus
Treatment/Control

Back 299

-symptomatic therapy
-clindamycin recommended for symptoms
-No antibiotics recommended for food poisoning

Front 300

M. leprae
General Info

Back 300

Similar to m. tuberculosis. Occur in epitheliod structures called lepra cells. Arrangements described as cigar packets

Front 301

M. leprae
Pathogenesis

Back 301

Ability to replicate in macrophages and host cells. Chronic inflammatory dz that ranges between two forms

Front 302

M. leprae
Clinical Manifestations

Back 302

Tuberculoid leprosy: cellular immunity partially effective. Localized dz. Slow progression, primarily affects skin and nerves

Lepromatous form: Generalized with massive # of skin lesions. More acute, associated with masses or granular tissue. Distortion and mutilation occur

Front 303

M. leprae
Epidimiology

Back 303

12 million individuals worldwide. Humans and armadillos are only hosts. Incubation periods quite long. Transmission is direct, person to person

Front 304

M. leprae
Diagnosis

Back 304

Never successfully cultivated on artificial media. Look at the skin! Endemic areas give clues to pathology

Front 305

M. leprae
Treatment/Control

Back 305

Dapsone

Rifampin

Ethionamide

Life long

NOT HIGHLIGHTED

Front 306

ERYSIPELOTHRIX
General Info

Back 306

G+ non-spore forming non-motile rods. Pleomorphic and may appear as coccobacilli

Front 307

ERYSIPELOTHRIX
Pathogenesis

Back 307

Enters a break in the skin, remains at site, localized. Erysipeloid rash resembles that from strep.

Front 308

ERYSIPELOTHRIX
Clinical Manifestations

Back 308

Erysipelas: Lesions characterized by a sharply defined painful purple red zone that advances peripherally. Bacteria fond at leading edge.

Front 309

ERYSIPELOTHRIX
Epidimiology

Back 309

Carried by turkeys, cattle, mice, fowl, swine and FISH

Survives in soil for years.

Occupational dz of slaughterhouse workers, fish handlers, veterinarians, and others who have animal exposure

Front 310

ERYSIPELOTHRIX
Diagnosis

Back 310

Chocolate agar culture

Front 311

ERYSIPELOTHRIX
Treatment/Control

Back 311

PCN

Cephalosporins

Front 312

M. Avium-intracellularae
General Info

Back 312

Atypical mycobacterium. Cause clinical illnesses in individuals with damaged tissues. No apparent case-to-case transmission. MORE RESISTANCE. Rapid growth and pigmentation

Front 313

M. Avium-intracellularae
Epidimiology

Back 313

Immunocompromised patients at risk.

Front 314

M. Avium-intracellularae
Diagnosis

Back 314

Culture, isolation, and biochemical tests

Front 315

M. Avium-intracellularae
Treatment/Control

Back 315

Azithromycin

Clarithromycin

Amikacin

NOT HIGHLIGHTED

Front 316

M. Avium-intracellularae
Clinical Manifestations

Back 316

Sole agents of TB like dz

Granulomatous cutaneous dz

Other skin infections involving necrotizing ulcers

Front 317

Corynebacterium
General Info

Back 317

Slender G+ but variable non motile, non encapsulated rods. Often club shaped or beaded with irregular staining granules, Chinese letter cell shapes

Front 318

Corynebacterium
Epidimiology

Back 318

Maintained in humans, the only hoist.

Endemic and epidemic in nature. Uncommon in US

Person to person droplet transmission

Highest incidence in unimmunized kids

Large incidence in underdeveloped countries

Front 319

Corynebacterium
Treatment/Control

Back 319

PCN
EMYCIN

VACCINE: formaldehyde treated toxin incorporated as part of DPT

Front 320

Corynebacterium
Clinical Manifestations

Back 320

Abrupt onset with fever and sorethroat. Lymphadenopathy common. Bullneck appearance followed by circulatory dysfunction and soft palate paralysis

Skin diphtheria largely confined to tropics. Chronic spreading ulcer covered by gray membranes.

Front 321

Nocardia
General Info

Back 321

G+, partially acid fast, non-spore forming bacillus. Filamentous and branching. Colonies are irregular and waxy. Variety of pigmentation

Front 322

Nocardia
Pathogenesis

Back 322

Chronic pneumonia follows inhalation. CNS involvement and dissemination from lungs can occur

Front 323

Nocardia
Epidimiology

Back 323

Systemic pulm. Infection acquired by airborne mycelia. Occasionally ingestion of contaminated food may initiate infection. Patients often immunosuppressed.

Front 324

Nocardia
Diagnosis

Back 324

Microscopic exam should demonstrate delicate filaments

Front 325

Nocardia
Treatment/Control

Back 325

Sulfonamidess

Front 326

M. tuberculosis
General Info

Back 326

Acid fast, G+ but difficult to stain. Slender slightly curved rods that may show filamentous branching. Acid fast stain a function of lipid content

Front 327

M. tuberculosis
Epidimiology

Back 327

2 billion people worldwide. Higher incidents with AIDS patients. Airborne transmission. Low infections dose required to initiate infection. Disease prevalent in underdeveloped countries. Humans are important source of infection

Front 328

M. tuberculosis
Diagnosis

Back 328

X-ray, sputum stain. Complex process involving isolation from specimen, digestive agents to liquefy tubercle, and biochemical tests. PCR available but LONG generation time.

TB skin test to screen for exposure. + test is a raised, > 5mm indurated lesion. + test requires CXR follow up

Front 329

M. tuberculosis
Treatment/Control

Back 329

Often synergistic drugs required

Isoniazid

Streptomycin
Rifampin

PROLONGED TX COURSE

Front 330

M. tuberculosis
Clinical Manifestations

Back 330

Pulmonary form is most common and accounts for 90% of death. S/S include fever, night sweats, anorexia, coughing, weight loss, long duration

Front 331

Listeria monocytogenes
General Info

Back 331

-Small G+ cocco bacilli with flagella

-Wide temp. range (.4-50 C)
-Growth at 2.5-4 C (refrigertion temps)

Front 332

L. monocytogenes
Pathogenesis

Back 332

Strains capable of hemolysis appear to be virulent. Listeriolysin disrupts membranes of host cells and required for infection.

Possess endotoxin like sfc component which demonstrate biologic and chemical similarity to LTS

Comet tails characteristic. Movement from cell to cell by actin tails. Invasion of cell membranes via phospholipases?

Front 333

L. monocytogenes
Epidimiology

Back 333

High epidemiology in immunocompromised hosts. Widely distributed in domestic animals, birds, fish, plants, soil.

Foods are most common vehicles for transmission because Refrigeration does not inhibit growth.

Front 334

L. monocytogenes
Diagnosis

Back 334

Blood or CS fluid. Gram stain usually negative due to small # of organisms isolated.

Pre or post natal infections, specimens isolated from GU tract.

Front 335

L. monocytogenes
Treatment/Control

Back 335

Ampicillin with or without gentamycin

SMZ-TMP
Sulfamethoxazole/trimethoprim

Front 336

L. monocytogenes
Clinical Manifestations

Back 336

Adult meningitis

Bacteremia

Neonatal listeriosis. Early onset causes stillbirth and death. Late onset involves meningitic signs in 3rd/2nd week of life. Mothers present with influenza like symptoms or are asymtomatic

Front 337

Actinomyces
Clinical Minifestations

Back 337

-Actinomycosis term for disease of these bacteria
-Most cases are cervicofacial
->other forms are thoracic, abdominal, pelvic, and CNS

Front 338

Actinomyces
Treatment

Back 338

-Drainage of infected areas and perhaps surgical excision
-antibiotics

Front 339

Peptostreptococcus
General Info

Back 339

-G+ cocci
-Anaerobic
-# of taxonomic groups that are all part of normal flora of->oral cavity, GI tract, GU tract, and skin

Front 340

Peptostreptococcus
Pathogenesis

Back 340

-infections involve seeding of a traumatized area

Front 341

Peptostreptococcus
Clinical Manifestations

Back 341

1.Brain abscess
2.Pleuropulmonary infections: lung abscess, necrotizing pneumonia, and empyema
3.skin and soft tissue infections
4.peritonitis and intraabdominal abscess

Front 342

Peptostreptococcus
Epidimioliogy

Back 342

In compromised hosts w/ disrupted natural defense barriers->skin and mucosa membranes

Front 343

Bacteriodes fragilis
Treatment

Back 343

-surgical therapy- drainage, excisision of necrotic tissue, resection of infected veins

-Antibiotics for anaerobic bacteria->metronidazole
-B-lactamase produced by most strands
-Hyperbaric oxygen is used

Front 344

Fusobacterium nucleatum
Treatment

Back 344

-surgical therapy- drainage, excisision of necrotic tissue, resection of infected veins

-Antibiotics for anaerobic bacteria->metronidazole
-B-lactams are more effective than in b. fragilis
-Hyperbaric oxygen is used

Front 345

Fusobacterium nucleatum
Diagnosis

Back 345

-foul odor of discharge, tissue necrosis and gas

-gram stain and BCH ID

Front 346

Haemophilus aphrophilus
General Info

Back 346

1) G-

2) normal flora

Front 347

Haemophilus aphrophilus
Clinical Manifestations

Back 347

Subacute endocarditis

(Is H in HACEK)

Front 348

Actinobacellus
General Info

Back 348

Part of normal oropharyngeal flora

Front 349

Actinobacellus
Clinical Manifestations

Back 349

-juvenille and adult periodontitis

-subacute endocarditis

(A in HACEK)

Front 350

Enterobacteriaceae
General Info

Back 350

1) Normal flora of intestinal tract

2)small; G- with fibriae and flagella

3)falcultative anaerobes

Front 351

Enterobacteriaceae
Pathogenesis

Back 351

Virulence factors
-endotoxin
-capsules
-antigenic phase variation
-exotoxin production
-adhesisons
-antimicrobial resistance

Front 352

Enterobacteriaceae
Clinical mANIFESTATIONS

Back 352

-40% of all noncosimal infections
-E. Coli causes 40% of neonatal meningitis
-E. Coli also causes- urethrocystitis, chronic bacterial prostatis, and acute pyelonephritis
-e.coli, proteus, klebsilla, and enterobacter most frequent causes of UTI
-Proteus->causes kidney stones
-Klebisiella pneumoniae- causes primary pneumonia
-Klebisilla granulomatis- causes granuloma inguinale-> STD in carribean

Front 353

Enterobacteriaceae
Epidemiology

Back 353

-noncosimal infections
-water, soil, intestinal tracts of humans and animals
-exogenous or endogenous
-indirecct transmission, can be on a number of vehicles

Front 354

Aeromonas
Info

Back 354

-Found in soil, fresh and marine water, sewage, marine animals
--causes diarrheal disease, wound infections, osteomyelitis, septicemia, maningitis

Front 355

Vibrio vulnificus
Diagnosis

Back 355

Postive blood culture and BCH tests

Front 356

Vibrio vulnificus
Treatment

Back 356

Wound debridement and antibiotic treatment

Front 357

Burkholderia cepacia
Clinical Manifestations

Back 357

1. respiratory tract in cystic fibrosis patients
2.UTI in catherized pts.
3.septicemia, partic. w/ pts. with contaminated catheters

Front 358

Burkholderia pseudomallei
Clinical Manifestations

Back 358

Meliodosis

-endemic to SE Asia, India, Africa, and Australlia

Front 359

Moraxella
Treatment

Back 359

Antibiotics

Front 360

Acinetobacter
Clinical Manifestations

Back 360

Infections include:
-Respiratory Tract infections
-Urinary Tract
-Wounds

Front 361

Bartonella bacilliformis
General

Back 361

1) Gram neg. bacilli
2) Causes Oroya fever
3) Due to a sandfly vector
4)Endemic to Peru, Ecuador, Columbia

Front 362

Bartonella Quintana
General

Back 362

1)G-
2)Trench fever, subacute endocarditis, bacillary angiomatosis
3)transmitted by a body louse
4)Aids patients (immunocompromised)

Front 363

Eikenella corrodens
General

Back 363

-E in HACEK
-normal flora of the oral cavity and upper respiratory tract
-Causes oppurtunistic infections
-Less comonly endocarditis, sinusitis, meningitis, brain abscess, pneumonia, and lung abscess
-Commonly From human bite wound or fistfight injury

Front 364

Streptobacillus moniliformis
General

Back 364

-Causes rat-bite fever, worldwide distribution
-Symptoms include myalgia, arthralgia, and arthritis
-Occur in nasopharynx of rats and other small rodents

Front 365

R. akari
General Info

Back 365

causes rickettsialpox

Front 366

Orientia tsutsugamushi
General Info

Back 366

causes scrub typhus

Front 367

Anaplasma phagocytophilum
General

Back 367

-obligate intracellular bacteria
-agent fo human anaplasmosis

Front 368

Chlamydiae
Pathogenesis

Back 368

1. attachement and penetration of an elementary body into a host cell

2.decvelopment of the elemental body into a reticulate body with a phagosome

3.Maturation of the reticulate body and formation of new elementary bodies

Front 369

Chlamydiae trachomatis
Pathogenesis

Back 369

1)Bacteria gain acess through small abraisons-granuloma formation
2)Lesions may become necrotic and attract PMN's and cause inflammation to surrounding tissues

Front 370

Mycoplasmas & Ureaplasmas
Treatment

Back 370

-do not use B-lactam
-agents that inhibit cell wall synthesis are not effective