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Clostridium Perfringens
General Info
-G+ Rods, very few spores
-Aerotolerant
-5 serologic types (A-E)
*A = major pathogen
Clostridium Perfringens
Pathogenesis
-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
Clostridium Perfringens
Clinical Manifestations
-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
Clostridium Perfringens
Epidemiology
-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
Clostridium Perfringens
Diagnosis
-early needed by clinical symptoms
-confirm with gram stain and culture
-spores are rare
-Nagler Test for  toxin
Clostridium Perfringens
Treatment Control
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
Clostridium Difficile
General Info
-G+ rods, Obligate Anaerobe
Clostridium Difficile
Pathogenesis
-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
Clostridium Difficile
Clinical Manifestations
-D, colitis, or pseudomembranous colitis
Clostridium Difficile
Epidemiology
-source is endogenous or exogenous
-risk factors: antibiotic exposure, older age, female sex, impaired intestinal motility
-varies with degree of hospital contamination
Clostridium Difficile
Diagnosis
-observe pseudomembrane with colonoscope
-ID toxin B in stools w/ EIA (not +)
-isolation from stools
-Must use a combination of the above for ID
Clostridium Difficile
Treatment Control
-discontinue use of drug
-maintain fluids + electrolyte balance
-avoid drugs that slow intestinal motility
-vancomycin
-untreated mortality rate of PC is high (27-44%)
Clostridium Tetani
General Info
-G+ rods
-Obligate Anaerobe
-Drumstick shaped with peritrichous flagella and terminal spore
Clostridium Tetani
Pathognesis
-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)
Clostridium Tetani
Clinical Manifestations
-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
Clostridium Tetani
Epidemiology
-sporadic disease
-rare in developed countries
-top 10 in others
-spores in soil
Clostridium Tetani
Diagnosis
-clinical symptoms
-organism can be recovered from the wound in only 1/3 of cases
-DD -> strychnine poisoning and encephalitis
Clostridium Tetani
Treatment Control
-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
Clostridium Botulinum
General info
-G+ rods
Clostridium Botulinum
Pathonogenesis
-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
Clostridium Botulinum
Clinical Manifestations
-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
Clostridium Botulinum
Epidimeology
-food-borne
-worldwide in soil and GI of birds, fish and mammals
-humans susceptible to A, B and E
-honey implicate in infant botulism
Clostridium Botulinum
Diagnosis
-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
Clostridium Botulinum
Treatment Control
-stomach lavage and high enemas
-antitoxin good if used early
-ventilatory assistance maybe
-Infant Botulism -> supportive care, do not use oral antibiotics
Actinomyces
General Info
-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
Actinomyces
Pathonogeneis
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
Actinomyces
Epidimiology
-direct introduction of organism into injured tissue or endogenous infection
-NO case to case transmission
-higher infection rate in men
Actinomyces
Diagnosis
-microscopic exam to see granules in clinical specimens
-crush granules and look for G+, nonacid-fast bacilli
-culture and BCH tests
Proprionibacterium
General Info
-G+ bacilli
-anaerobic
-commonly on skin surface
-P. acnes
Proprionibacterium
Pathonogenesis
-bacterium stimulates an inflammatory response that results in rupture of sebaceous follicles
Proprionibacterium
Clinical Manifestations
P. acnes causes acne & opportunistic infections
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Proprionibacterium
Treatment Control
For acne-Topical benzoyl peroxide & erythromycin
Bacteriodes Fragilis
General Info
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
Bacteriodes Fragilis
Clinical Manifestations
-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
Bacteriodes Fragilis
Epidimiology
-endogenous infection
-found in oral cavity, GI tract, vagina and urethra
Bacteriodes Fragilis
Diagnosis
-foul odor of discharge, tissue necrosis and gas
-gram stain and BCH ID
Fusobacterium Nucleatum
General Info
1) G-

2)long rods with thin pointed ends (fusiform)
- < ox/red potential or GI trauma predispose
Fusobacterium Nucleatum
CLinical Manifestations
-seen most commonly in oral infections, lung abscesses, and pleuropulmonary infections
-mixed infection with spirochetes -> Vincent’s Angina and Trench Mouth
Fusobacterium Nucleatum
Epidimiology
-endogenous infection
-found in oral cavity and urogenital tract
-Some found in GI tract
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Pasteurellaceae: Haemophilus
General Info
-Small to medium sized G- coccobacilli or rods
-many strains posses capsules
Pasteurellaceae: Haemophilus
Pathogenesis
-all require either 1 or both growth factors present in the blood:
1. X factor = hematin
2. V factor = NAD
Pasteurellaceae: Haemophilus
Epidimiolgy
-satellite phenomenon with staphylococci
Pasteurellaceae: Haemophilus
Diagnosis
-chocolate agar used as a culture medium
-X & V factors released when blood heated and cells lyse
Haemophilus Influenzae
General Info
- G-, pleomorphic
-6 capsular types (a-f)
-95% of invasive disease by b
Haemophilus Influenzae
Pathogenesis
-virulence factors: LPS and capsules (PRP – antiphagocytic)
-POE is the respiratory tract
Haemophilus Influenzae
Clinical Manifestations
-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)
Haemophilus Influenzae
Epidimiology
-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
Haemophilus Influenzae
Diagnosis
-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
Haemophilus Influenzae
Treatment/Control
-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
Haemophilus Aegyptius
General Info
- G-, pleomorphic
Haemophilus Aegyptius
Clinical Manifestations
Purulent conjunctivitis known as “pink eye”
Haemophilus Aegyptius
Epidimiology
Occurs in hot climates
Haemophilus Aegyptius
Treatment/Control
Topical sulfonamides
Haemophilus Ducreyi
General Info
- G-, pleomorphic
Haemophilus Ducreyi
CLinical Manifestations
-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
Haemophilus Ducreyi
Epidimiology
-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
Haemophilus Ducreyi
Diagnosis
-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
Pasturella
Treatment/Control
Ampicillin or Tetracycline
Pasturella
General Info
- G- coccobacilli
-P. Multocida and P. canis are the major human pathogens
Pasturella
Pathogenesis
-localized abscesses associated with cat or dog bites
-especially in wounds that have been sutured
Pasturella
CLinical Manifestations
-regional lymphadenitis, discoloration, severe local pain and swelling
-2nd most common form is infection of lung with preexcisitng chronic pulmonary disease
Pasturella
Epidimioloy
-normal flora of many domestic animals
-transmission by a bite
-animal reservoirs are asymptomatic
Pasturella
Diagnosis
Isolation from clinical specimen, blood, sputum, or exudate from animal bites
Bordetella Pertussis
General Info
1)G-
2)coccobacilli
3) extremely small
4)obligate aerobes

-Species that most commonly causes serious human infections

-bipolar metachromatic staining
Bordetella Pertussis
Pathogenesis
-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
Bordetella Pertussis
Clinical Manifestation
-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
Bordetella Pertussis
Epidimiology
-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
Bordetella Pertussis
Diagnosis
-isolation during catarrhal stage
-streak plate with nasopharyngeal swab passed through penicillin or cephalosporin
-BCH ID and use PCR
Bordetella Pertussis
Treatment/Contol
-immune human globin early in disease for infants < 2yrs
-supportive (suction for secretions, hydration)
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Francisella Tularensis
General Info
-causes tularemia = rabbit fever, tick fever, deer fly fever, and glandular fever
->G- coccobacillus
-very small
Francisella Tularensis
Pathogenesis
-intracellular parasite – survives a long time in Macrophages-inhibits phagosome/lysosome function
Francisella Tularensis
Clinical Manifestation
-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
Francisella Tularensis
Epidimiology
-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
Francisella Tularensis
Diagnosis
-specimen processing hazardous
-lab acquired infections are common
Moraxella
General Info
- G- bacilli
-M. Catarrhalis
-part of normal flora of the upper respiratory tract
Moraxella
Clinical Manifestations
-significant agent of otitis media in children
-other infections: bronchitis, sinusitis, and bronchopneumonia
Moraxella
Epidimiology
-normal flora of URT
Acinetobacter
General Info
- G- bacilli
-occurs as an opportunistic pathogen
Acinetobacter
Epidimiology
-primarily in comprimised pts.
-common cause of nosocomial respiratory infections
-likes moist environments
-contaminants of respiratory equipment
Escherichia Coli
General Info
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
Escherichia Coli
Pathogenesis/ Clinical Manifestations
-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
Escherichia Coli
Epidimeology
-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
Escherichia Coli
Diagnosis
-assay by nucleic acid probe for enterotoxins or presence of toxin genes on plasmids (more common)
-serology for epidemiology
Neisseria Meningitidis
Treatment/Control
1) meniingitis and meningoccemia- Ceftriaxone

2)Polyvalent capsular vaccine
-> people older than 65 and international travelers
3)Conjugate vaccine (Menactra)
Neisseria Meningitidis
General Info
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
Neisseria Meningitidis
Pathogenesis
-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
Neisseria Meningitidis
Clinical Manifestations
-mild febrile disease w/ or w/o pharyngitis
-pneumonia
-fulminating meningococcemia
-meningitis
Neisseria Meningitidis
Epidimiology
-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
Neisseria Meningitidis
Diagnosis
-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
Neisseria Gonorrhoeae
General Info
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
Neisseria Gonorrhoeae
Pathognesis
-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
Neisseria Gonorrhoeae
Clinical Manifestations
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
Neisseria Gonorrhoeae
Epidimeology
-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
Neisseria Gonorrhoeae
Dianosis
-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
Neisseria Gonorrhoeae
Treatment/Control
-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
Salmonella
General Info
-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
Salmonella
Pathogenesis
ability to grow withion M cells of peyers patches nad nonactivate macrophages
Salmonella
Clinical Manifestations
-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
Salmonella
Epidimiology
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
Salmonella
Diagnosis
-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)
Salmonella
Treatment/ Control
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
Shigella
General Info
-G-, nonmotile (no flagella)
-facultative anaerobic
-no H2S & no gas
-bile inhibits it
-S. Dysenteriae
-S. Flexneri
-S. Sonnei
Shigella
Pathogenesis
-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
Shigella
Clinical Manifestations
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
Shigella
Epidimiology
-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
Shigella
Diagnosis
-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
Shigella
Treatment/Control
-treat dehydration and fever
-treat infections with antibiotics
-safe water supply, sewage treatment, handwashing
-reportable disease
Yersinia Enterocolitica
General Info
-G-, enveloped coccobacilli w/ bipolar staining
-causes severe gastrointestinal infections (enterocolitis)
Yersinia Enterocolitica
Pathogenesis
> metabolic activity @ 22-25 degrees C
Yersinia Enterocolitica
Clinical Manifestation
-primarily in colder areas of North America (22-25 deg. C)
-water, milk, wild and domestic animals
-milk and contaminated meat linked to epidemics
Yersinia Pestis
General Info
-G-, enveloped coccobacilli w/ bipolar staining
-causes bubonic and pneumonic plague
Yersinia Pestis
Pathogenesis
-protein polysaccharide capsule is antiphagocytic
-heat-labile exotoxin (murine toxin) acts on mitochondria
-Pimary lesion and infection @ site of flea bite
Yersinia Pestis
Clinical Manifestations
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
Yersinia Pestis
Epidimiology
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
Yersinia Pestis
Diagnosis
-blood, sputum, lymph node biopsy
-clinical specimens hazardous
-FA, guinea pig inoculation
-send to appropriate lab for ID
Yersinia Pestis
Treatment/Control
-antibiotic (streptomycin) therapy w/in 12-15 hours after appearance of fever
-vaccine available for researchers and travelers
-quarantinable disease
Vibrio Cholerae
General Info
-G- straight or curved rods (comma-shaped)
-monotrichous or lophotrichous flagella
-Na ions increase growth rate
-O Ag for grouping
Vibrio Cholerae
Pathogenesis
-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
Vibrio Cholerae
Clinical Manifestation
-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)
Vibrio Cholerae
Epidimiology
-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
Vibrio Cholerae
Treatment/Control
-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
Vibrio Vulnificus
General Info
-G- straight or curved rods (comma-shaped)
-monotrichous or lophotrichous flagella
-Na ions increase growth rate
-O Ag for grouping
Vibrio Vulnificus
Clinical Manifestations
-wound infections and septicemia
-mild infection to severe cellulitis
-bullous skin lesions
Vibrio Vulnificus
Epidimiology
-fresh water or salt water (estuaries or coastal waters)
-occurs after ingestion of raw or poorly cooked seafood
-MR as high as 20-50%
Campylobacter Jejuni
General Info
- 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
Campylobacter Jejuni
Clinical Manifestations
-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
Campylobacter Jejuni
Epidimeology
-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
Campylobacter Jejuni
Diagnosis
-isolation and ID w/ BCH
-specialized media
-> Campy BAP
-Decrease [O2] @ 42 degrees C
*slow growers (48-72 hrs)
Helicobacter Pylori
General Info
G- spiral shaped or gull-winged with 6 polar sheathed flagella
Helicobacter Pylori
Pathogenesis
-increased by motility, urease, adhesins, LPS, and vacuolating cytotoxin & cagA
-resides in the stomach or occasionally the esophagus
Helicobacter Pylori
Clinical Manifestations
-gastritis and development of gastric or peptic ulcers
-gastric adenocarcinoma
-b cell lymphomas
Helicobacter Pylori
Epidimiology
-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
Helicobacter Pylori
Diagnosis
-ELIZA for IgG or IgA in saliva or plasma
-gastric biopsy, isolation and cultivation, urease test
-urea breath test (oral 14C)
-PCR
Helicobacter Pylori
Treatment/Control
-2 or 3 antimicrobials (amoxicillin plus metronidazole or bismuth subsalicylate)
-1 antib + antisecretory agent (histrionic H2 antagonist) has had poor results
Brucella
General Info
-causes Brucellosis = undulant fever = malta fever, Bangs Disease (cattle)
-B. Melitensis
-> G- ; coccobacilli
Brucella
Pathogenesis
-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
Brucella
Clinical Manifestation
-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
Brucella
Epidimiology
-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
Brucella
Diagnosis
-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
Brucella
Treatment/Control
-vaccine for animals
->eliminates human disease
Pseudomonas
General Info
- 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
Pseudomonas
Pathogenisis
-biofilm development
-alginate synthesis
-LPS
-antibiotic resistance
Pseudomonas
Clinical Manifestation
-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
Pseudomonas
Epidimiology
-present everywhere
-common in hospitals
-pt to pt transmission
-food and water contamination
Pseudomonas
Diagnosis
-various testing after isolation
-blue-green pigment, grape-like odor
Pseudomonas
Treatment/Control
-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)
Stentrophomonas Maltophilia
General Info
-looks like pseudomonas
- non-sporulating G- bacilli w/ polar flagella
Stentrophomonas Maltophilia
Pathogenesis
-affected by ability to adhere to plastic, glass and Teflon and to survive and multiply in various types of IV insulfates
Stentrophomonas Maltophilia
Clinical Manifestations
-bacteremia, endocarditis, RT infection, CNS infection, opthalmologic, UTI, skin and soft tissue infection, bone and joint infection, and GI infection
Stentrophomonas Maltophilia
Epidimiology
-isolated from nosocomial sources (blood tubes, dispensers, dialysis, disinfectant, shower heads, faucets, personnel’s hands)
-human carriage ???
Stentrophomonas Maltophilia
Treatment/Control
-resistance is a problem with antibiotics
-penicillins and cephalosporins are ineffective
Legionella Pneumophilia
General Info
- G- bacilli, poorly staining
-obligate aerobes
-req. charcoal yeast medium
-slow growers
-primary human pathogen
Legionella Pneumophilia
Pathogenesis
-facultative intracellular parasites in Macrophages
-prevents lysosome-phagosome function
-survives in biofilms and protozoans
Legionella Pneumophilia
Clinical Manifestations
-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
Legionella Pneumophilia
Epidimiology
-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
Legionella Pneumophilia
Diagnosis
-DFA, take aspirate and test
ELISA, RIA, indirect FA
-difficult to send specimens to lab (infectious)
Legionella Pneumophilia
Treatment/Control
-erythromycin or rifampin
-maybe O2 therapy, nasoactive drugs and/or renal dialysis
-control by cleaning air conditioning systems
-hyperchlorinate water
Treponema pallidum
General Info
-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
Treponema pallidum
Pathogenesis
-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
Treponema pallidum
Clinical Manifestations
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
Treponema pallidum
Epidimiology
-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)
Treponema pallidum
Diagnosis
-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
Treponema pallidum
Treatment/Control
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
Borrelia
General Info
1)G- spirochete
-B. Burgdorferi* (Lyme Ds) & B. Recurrentis** (relapsing fever)

* = minor Ag shifts
** = major Ag shifts
Borrelia
Clinical Manifestations
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
Borrelia
Epidimiology
-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)
Borrelia
Diagnosis
-IFA is the best test
-also ELISA and PCR
-demonstration of bacteria in blood
Borrelia
Treatment/Control
Tetracycline
Leptospira interrogans
General Info
-Weil’s Disease AKA leptospirosis
-G- helical spirochetes w/ hooked ends
-multilayered outer envelope
Leptospira interrogans
Pathogenesis
-no toxins
-invasion is via mucosa & broken skin
-no lesion at the site of entry
Leptospira interrogans
Clinical Manifestations
-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
Leptospira interrogans
Epidimiology
-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
Rickettsia
General Info
-G- coccobacilli
-obligate intracellular parasites w/ long generation time
Rickettsia
Pathogenesis
-Induce phagocytosis and enter endothelial cells
-replicate in cytoplasm or nucleus of host cells
Rickettsia
Clinical Manifestations
-Induce phagocytosis and enter endothelial cells
-replicate in cytoplasm or nucleus of host cells
CLASSIC TRIAD OF DISEASES -> Fever, headache & rash
R. Rickettsii
General Info
Etiologic agent of rocky mountain spotted fever (RMSF)
R. Rickettsii
Pathogenesis
-widespread endothelial damage w/ occlusion of small vessels, microhemorrhages, electrolyte changes and perhaps necrosis, shock and death
R. Rickettsii
Clinical Manifestation
-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
R. Rickettsii
Epidimiology
-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
R. Rickettsii
Diagnosis
-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
R. Rickettsii
Treatment/Control
Antibiotic treatment Should begin immediately
R. Prowazekii
Causes epidemic typhus
R. Typhi
Causes murine typhus
Coxiella burnetii
General Info
1) G-, obligate intracellular bacterium
-Etiologic agent of Q fever
-highly resistant to heat, cold, sunlight, drying, & chemicals (unique)
Coxiella burnetii
Clinical Manifestations
-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
Coxiella burnetii
Epidimiology
-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
Ehrlichia chaffensis
General Info
Etiologic agent of human monocytic Ehrlichiosis

-obligate intracellular bacteria
Ehrlichia chaffensis
Clinical Manifestations
-fever, headache, malaise, & myalgia
-rash in 30-40%
-leukopenia andthrombocytopenia occur
Ehrlichia chaffensis
Epidimiology
Transmission via ticks
Bartonella Henselae
General Info
G- bacilli
-Causes cat scratch disease
Bartonella Henselae
Clinical Manifestations
-Bacillary angiomatosis
-Cat Scratch Fever- fever, lymphadenopathy, & osteolytic lesions
-Subacute endocarditis
Bartonella Quintana
Epidimeology
-AIDS pts
Bartonella Henselae
Treatment/Control
antibiotics
Chlamydiae
General Info
-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
C. Trachomatis
Clinical Manifestations
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
C. Trachomatis
Epidimiology
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
C. Trachomatis
Diagnosis
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
C. Trachomatis
Treament/Control
NONGON G/R INF
-azithromycin
-doxycycline
-erythromycin
-ofloxicin
-Tx for gonorrhea as well
LGV
-azithromycin
-doxycycline
C. Psittaci
General Info
-causes psittacosis or ornithosis
C. Psittaci
Epidimiology
-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
C. Pneumoniae
Clinical Manifestations
-acute RT infections  sinusitis & bronchitis (walking pneumonia)
C. Pneumoniae
Epidimiology
-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
C. Pneumoniae
Diagnosis
-NAAT's
-EIA, DFA for Ag, PCR
-microimmunoflourescence for serology
Mycoplasmas & Ureaplasmas
General Info
-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)
Mycoplasmas & Ureaplasmas
Pathogenesis
M PNEUMONIAE
-no toxins
-adhere specifically to epithelial cells  interfere with ciliary actions -> stimulate an inflamm reaction and exudate
Mycoplasmas & Ureaplasmas
Clinical Manifestations
-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
Mycoplasmas & Ureaplasmas
Epidimiology
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
Mycoplasmas & Ureaplasmas
Diagnosis
-microscopy sucks b/c organisms are too small
-serologic tests: MIF, cold agglutinins test
Mycoplasmas & Ureaplasmas
Treatment/Control
Doxycycline & erythromycin
Staph aureus
General Info
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
Staph. aureas
Pathogenesis
Cytolytic toxins(alpha toxin- lyse RBC's), Enterotoxins- cause food poisoning, Exfoliative Toxins- Cause Scalded Skin Syndrome, TSST-1- causes TSS
Staph. aureus
Clinical Manifestations
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
Staph aureus
Epidimiology
-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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Staph aureus
Diagnosis
-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
Staph aureus
Treatment/Control
-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
Streptococcus
General Info
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
Streptococcus
Clinical Manifestations
-in bloodstream, respiratory tract & skin infections
-post-infection problems w/ rheumatic fever & glomerulonephritis
Group A Strep (Streptococcus pyogenes) (GAS)
Pathogenesis
-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
Group A Strep (Streptococcus Pyrogenes) (GAS)
Clinical Manifesations
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
Group A Strep (Streptococcus Pyrogenes) (GAS)
Epidimiology
-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
Group A Strep (Streptococcus Pyrogenes) (GAS)
Diagnosis
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
Group A Strep (Streptococcus Pyrogenes) (GAS)
Treatment/control
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
Group B Strep (Streptococcus agalactiae) (GBS)
General Info
leading cause of neonatal sepsis & meningitis
Group B Strep(Streptococcus agalactiae) (GBS)
Clinical Manifestations
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
Group B Strep(Streptococcus agalactiae) (GBS)
Epidimeology
-normal flora of pharynx, GI tract, & vagina

1-3 neonatal cases per 1000 births
Group B Strep(Streptococcus agalactiae) (GBS)
Treatment/Control
Ampicillin plus Gentamycin for neonates
Viridans Strep
General Info
-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
Viridans Strep
Pathogenesis
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)
Viridans Strep
Clinical Manifestations
Causes SBE, meningitis, sinusitis, intra-abd infections
Viridans Strep
Treatment/Control
Penicillin + aminoglycoside (streptomycin)
Strep Pneumoniae
General Info
-Pairs of lancet shaped cells
-NO Lancefield Ags
-serotypes based on capsular Ag
-alpha hemolytic
-87% of pneumococcal disease in the US
Strep Pneumoniae
Pathogenesis
-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
Strep Pneumoniae
Clinical Manifestations
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
Strep Pneumoniae
Epidimiology
-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
Strep Pneumoniae
Diagnosis
-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
Strep Pneumoniae
TReatment/Control
-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)
Enterococcus
General Info
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)
Enterococcus
Clinical Manifestation
-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
Enterococcus
Epidimiology
-may originate from normal flora(large intestine and GU tratct)
-P->P transmission
-outbreaks among hospitalized neonates
Enterococcus
Diagnosis
Isolation and biochemical ID
 Bile-esculin positive
 growth in 6.5% NaCl
-Test for optochin sensitivity (Enterococcus is resistant)
Enterococcus
Treatment/Control
Test for antibiotic susceptibility

 Synergistic Tx being used

Antibiotics- Linezolid, and quinupristin/dalfopristin
Bacillus
General Info
-G+ rods that move by using peritrichous flagella
-Endospore formation
B. Anthracis
General Info
Causes Anthrax
-facultative anaerobe (12-45C)
B. Anthracis
Pathogenesis
-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
B. Anthracis
Clinical Manifestations
-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
B. Anthracis
Epidimiology
-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
B. Anthracis
Diagnosis
-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
B. Anthracis
Treatment/Control
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
B. Cereus
General Info
Causes Food Poisoning
B. Cereus
Clinical Manifestations
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
B. Cereus
Epidimiology
-most common cause of traumatic eye infections-> from soil contamination of object penetrating eye or direct inoculation
B. Cereus
Diagnosis
-clinical picture, gram stain, & biochemical ID
-food poisoning might involve isolation in food or
-detection of enterotoxin
B. Cereus
Treatment/Control
-symptomatic therapy
-clindamycin recommended for symptoms
-No antibiotics recommended for food poisoning
M. leprae
General Info
Similar to m. tuberculosis. Occur in epitheliod structures called lepra cells. Arrangements described as cigar packets
M. leprae
Pathogenesis
Ability to replicate in macrophages and host cells. Chronic inflammatory dz that ranges between two forms
M. leprae
Clinical Manifestations
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
M. leprae
Epidimiology
12 million individuals worldwide. Humans and armadillos are only hosts. Incubation periods quite long. Transmission is direct, person to person
M. leprae
Diagnosis
Never successfully cultivated on artificial media. Look at the skin! Endemic areas give clues to pathology
M. leprae
Treatment/Control
Dapsone

Rifampin

Ethionamide

Life long

NOT HIGHLIGHTED
ERYSIPELOTHRIX
General Info
G+ non-spore forming non-motile rods. Pleomorphic and may appear as coccobacilli
ERYSIPELOTHRIX
Pathogenesis
Enters a break in the skin, remains at site, localized. Erysipeloid rash resembles that from strep.
ERYSIPELOTHRIX
Clinical Manifestations
Erysipelas: Lesions characterized by a sharply defined painful purple red zone that advances peripherally. Bacteria fond at leading edge.
ERYSIPELOTHRIX
Epidimiology
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
ERYSIPELOTHRIX
Diagnosis
Chocolate agar culture
ERYSIPELOTHRIX
Treatment/Control
PCN

Cephalosporins
M. Avium-intracellularae
General Info
Atypical mycobacterium. Cause clinical illnesses in individuals with damaged tissues. No apparent case-to-case transmission. MORE RESISTANCE. Rapid growth and pigmentation
M. Avium-intracellularae
Epidimiology
Immunocompromised patients at risk.
M. Avium-intracellularae
Diagnosis
Culture, isolation, and biochemical tests
M. Avium-intracellularae
Treatment/Control
Azithromycin

Clarithromycin

Amikacin

NOT HIGHLIGHTED
M. Avium-intracellularae
Clinical Manifestations
Sole agents of TB like dz

Granulomatous cutaneous dz

Other skin infections involving necrotizing ulcers
Corynebacterium
General Info
Slender G+ but variable non motile, non encapsulated rods. Often club shaped or beaded with irregular staining granules, Chinese letter cell shapes
Corynebacterium
Epidimiology
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
Corynebacterium
Treatment/Control
PCN
EMYCIN

VACCINE: formaldehyde treated toxin incorporated as part of DPT
Corynebacterium
Clinical Manifestations
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.
Nocardia
General Info
G+, partially acid fast, non-spore forming bacillus. Filamentous and branching. Colonies are irregular and waxy. Variety of pigmentation
Nocardia
Pathogenesis
Chronic pneumonia follows inhalation. CNS involvement and dissemination from lungs can occur
Nocardia
Epidimiology
Systemic pulm. Infection acquired by airborne mycelia. Occasionally ingestion of contaminated food may initiate infection. Patients often immunosuppressed.
Nocardia
Diagnosis
Microscopic exam should demonstrate delicate filaments
Nocardia
Treatment/Control
Sulfonamidess
M. tuberculosis
General Info
Acid fast, G+ but difficult to stain. Slender slightly curved rods that may show filamentous branching. Acid fast stain a function of lipid content
M. tuberculosis
Epidimiology
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
M. tuberculosis
Diagnosis
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
M. tuberculosis
Treatment/Control
Often synergistic drugs required

Isoniazid

Streptomycin
Rifampin

PROLONGED TX COURSE
M. tuberculosis
Clinical Manifestations
Pulmonary form is most common and accounts for 90% of death. S/S include fever, night sweats, anorexia, coughing, weight loss, long duration
Listeria monocytogenes
General Info
-Small G+ cocco bacilli with flagella

-Wide temp. range (.4-50 C)
-Growth at 2.5-4 C (refrigertion temps)
L. monocytogenes
Pathogenesis
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?
L. monocytogenes
Epidimiology
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.
L. monocytogenes
Diagnosis
Blood or CS fluid. Gram stain usually negative due to small # of organisms isolated.

Pre or post natal infections, specimens isolated from GU tract.
L. monocytogenes
Treatment/Control
Ampicillin with or without gentamycin

SMZ-TMP
Sulfamethoxazole/trimethoprim
L. monocytogenes
Clinical Manifestations
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
Actinomyces
Clinical Minifestations
-Actinomycosis term for disease of these bacteria
-Most cases are cervicofacial
->other forms are thoracic, abdominal, pelvic, and CNS
Actinomyces
Treatment
-Drainage of infected areas and perhaps surgical excision
-antibiotics
Peptostreptococcus
General Info
-G+ cocci
-Anaerobic
-# of taxonomic groups that are all part of normal flora of->oral cavity, GI tract, GU tract, and skin
Peptostreptococcus
Pathogenesis
-infections involve seeding of a traumatized area
Peptostreptococcus
Clinical Manifestations
1.Brain abscess
2.Pleuropulmonary infections: lung abscess, necrotizing pneumonia, and empyema
3.skin and soft tissue infections
4.peritonitis and intraabdominal abscess
Peptostreptococcus
Epidimioliogy
In compromised hosts w/ disrupted natural defense barriers->skin and mucosa membranes
Bacteriodes fragilis
Treatment
-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
Fusobacterium nucleatum
Treatment
-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
Fusobacterium nucleatum
Diagnosis
-foul odor of discharge, tissue necrosis and gas

-gram stain and BCH ID
Haemophilus aphrophilus
General Info
1) G-

2) normal flora
Haemophilus aphrophilus
Clinical Manifestations
Subacute endocarditis

(Is H in HACEK)
Actinobacellus
General Info
Part of normal oropharyngeal flora
Actinobacellus
Clinical Manifestations
-juvenille and adult periodontitis

-subacute endocarditis

(A in HACEK)
Enterobacteriaceae
General Info
1) Normal flora of intestinal tract

2)small; G- with fibriae and flagella

3)falcultative anaerobes
Enterobacteriaceae
Pathogenesis
Virulence factors
-endotoxin
-capsules
-antigenic phase variation
-exotoxin production
-adhesisons
-antimicrobial resistance
Enterobacteriaceae
Clinical mANIFESTATIONS
-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
Enterobacteriaceae
Epidemiology
-noncosimal infections
-water, soil, intestinal tracts of humans and animals
-exogenous or endogenous
-indirecct transmission, can be on a number of vehicles
Aeromonas
Info
-Found in soil, fresh and marine water, sewage, marine animals
--causes diarrheal disease, wound infections, osteomyelitis, septicemia, maningitis
Vibrio vulnificus
Diagnosis
Postive blood culture and BCH tests
Vibrio vulnificus
Treatment
Wound debridement and antibiotic treatment
Burkholderia cepacia
Clinical Manifestations
1. respiratory tract in cystic fibrosis patients
2.UTI in catherized pts.
3.septicemia, partic. w/ pts. with contaminated catheters
Burkholderia pseudomallei
Clinical Manifestations
Meliodosis

-endemic to SE Asia, India, Africa, and Australlia
Moraxella
Treatment
Antibiotics
Acinetobacter
Clinical Manifestations
Infections include:
-Respiratory Tract infections
-Urinary Tract
-Wounds
Bartonella bacilliformis
General
1) Gram neg. bacilli
2) Causes Oroya fever
3) Due to a sandfly vector
4)Endemic to Peru, Ecuador, Columbia
Bartonella Quintana
General
1)G-
2)Trench fever, subacute endocarditis, bacillary angiomatosis
3)transmitted by a body louse
4)Aids patients (immunocompromised)
Eikenella corrodens
General
-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
Streptobacillus moniliformis
General
-Causes rat-bite fever, worldwide distribution
-Symptoms include myalgia, arthralgia, and arthritis
-Occur in nasopharynx of rats and other small rodents
R. akari
General Info
causes rickettsialpox
Orientia tsutsugamushi
General Info
causes scrub typhus
Anaplasma phagocytophilum
General
-obligate intracellular bacteria
-agent fo human anaplasmosis
Chlamydiae
Pathogenesis
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
Chlamydiae trachomatis
Pathogenesis
1)Bacteria gain acess through small abraisons-granuloma formation
2)Lesions may become necrotic and attract PMN's and cause inflammation to surrounding tissues
Mycoplasmas & Ureaplasmas
Treatment
-do not use B-lactam
-agents that inhibit cell wall synthesis are not effective