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Cocci Bacilli
CAT+ - Staph Spore forming
CAT- -Strep ANAEROBE: Clostridium species
Aerobe: Bacillus Species
Non-spore forming,
CAT +
CAT -
Impetigo, furuncles
Rhematic fever
Penicillinase Acute glomerulonephritis
Strep TSS
Food Poisoning
Erysipelas, cellulitis
.COCCI.
+ = S. Aureus*
- = S. epidermidis, S. saphrophyticus
CHARACTERISTICS
Facultative Anaerobe
Virulence factors
Protein A:
descending UTI
STAPH AUREUS - CAT+, COAG+
(hem. spread)
CYTOTOXINS
2) Pyrogenic Exotoxin
EXOTOXINS
IN INFANTS
MINOR pressure = Nikolskys sign (skin separation)
OTHER IMPLICATIONS
works on the gut receptors (vagus and sympathetic increased susceptibility in HIV patients
(diarrhea)
STAPH AUREUS ID
LiCL + Tellurite
detection level).
S. Epidermidis
SMB
BIOFILM PRODUCER!
S. Sapro -
UGI
UTI IN SEXUALLY ACTIVE FEMALES!
urease
S. Lugdunesis
SMB
A LOT like S. Aureus, can produce skin and soft tissue infections
ALPHA HEMOLYTIC
S. pneumonaiea (opt senstive, quelling +)
LAB ID
STREP PNEUMONIA
SPREAD via pores of KOHN
PATHOGENESIS:
RED HEPATIZATION: exudate w/ RBCs fibrin,
CARRIAGE: throat/nasopharynx
**VIRULENCE FACTORS PMNs, becomes SOLID
mouse model showed that teichoic and lipoteichoic acids help bind Ascho bodies seen in the heart
to neurons -- retrograde axonal transport up olfactory neurons can become chronic = MITRAL stenosis
*HUGE CONCERN TO AIDS PATIENTS re: Pneumonia! IMMUNE complex deposition in organs (ie
glomerulonephritis)
VACCINE!
***ENDOCARDITIS, Subacute
with CCa
BETA HEMOLYTIC
GROUP A
production
appearance on BA
B-hemolytic
small colonies without pigment
**BACITRACIN SENSITIVE, OPTOCHIN
RESISTANT!
Pen. Sus
VIRULENCE FACTORS
TOXINS PRODUCED
MANIFESTATIONS:
ERYSPELAS: Topical,
superficial lymph
CELLULITIS: accompanied
GROUP B
S. Agalactiae -
C. Dicile
Motile -> Listeria Monocytones
C. Botulinum
CATALASE -
C. perfringens
Erysipelothix
C. tetani
Lactobacillus
B. Anthracis
Nocardia
B. Cereus
Propionibacterium
SYSTEMS
CLOSTRIDIUM SPECIES - GI - all three
ANAEROBIC SKIN
ANAEROBIC
FERMENT CH20's
MOTILE!
SUSCEPTIBLE TO PEN.
Found in SOIL and GI
INFANT IS THE MOST COMMON "FLOPPY BABY SYNDROME"
3 TYPES: food, wound, infant
heart
Enterotoxin - CPE Noninflamm. GI
Other VF ID: Double zone of hemolysis
also use a milk medium which = fermentation
Collagenase, DNAse, hyaluronidase, protease
SKIN FOR GI: utilize Stool sample
post gun shot wounds/trauma - MEDICAL EMERGENCY
crepitations, and gas seen in X-rays
CELLULITIS, Endometrititis (seen in illegal abortions)
NEEDS DEBRIDEMENT IMMEDIATELY
GI: 2 forms - non inflamm
1) Necrotic enteritis (PAPUA NEW GUINEA) - strain C,
improperly cooked pork [RARE]
B. CEREUS - GI
lethal factor)
protective Ag
KEY WORDS: Farm,
edema, redness
2) GI
INCUBATION: 1-7days
B. CEREUS
Habitat = air, soil, water, and dust > easy to spread to food (aka why RICE IS
IMPLICATED) TO KNOW!
Contains emetic toxin and enterotoxin. Key = two types of gastroenteritis. (EMETIC and LT TOXIN: [HEAT LABILE A-B]
ENTEROTOXIN) Seen also in ETEC
B subunit uses GM1 as receptor
FOOD POISONING (EMETIC): RESEMBLES S. Aureus on enterocytes in SI -> Subunit A
ST TOXIN! (Neurotoxin) -- THROWING UP! enters the cell and ADP
Incubation time: 2-3 hours; duration 6-24 hours, QUICK!
FOODS: RICE RICE RICE - "chinese food syndrome" ribosylates Gs, inhibits GTPaase
and increasing cAMP levels
NON-inflam. Illness - (ENTEROTOXIN): Resembles C. perfringens increase cAMP opens CFTR =
LT [like E.COLI] : INCREASE IN CAMP --> increase in NaCL reabsorption - WATERY electrolyte and fluid loss!!
DIARRHEA!
FOODS: DAIRY! desserts, meats, veggies [DIFF WITH S. aureus BUT S. AUREUS will
happen quicker!!!) this will take longer
INCUBATION: 8-16 hours
ID on BA: DRY FLAT AND WRINKLY! (old man balls ID)
GRAM POSITIVE: BACILLI
NONE SPORE FORMERS!
1.2 NON SPORE FORMING, CAT + 1.3 NON SPORE FORMING, CAT -
ANAEROBES
C. Diptheria -- NOT IN POST MIDTERM Erysipelothrix rhusiopathiae - SMB
BUT WHY NOT - RESP FISHERMEN, butchers, Vets!
DIPHTHEROID LIKE RODS!
PATHOGENESIS - decreased protein synth
"CHINESE LETTERS"
NON-INVASIVE, does NOT enter bloodstream
Nocardia SIMILAR
Acitinomyces - SMB
Long, Gram (+ve) rod; not acid fast;
branching rods; Irregular, small white
fuzzy colonies. Uterine infection (IUD),
aspiration pneumonia, head/neck
abscess.
TOOTH CARIES!!!
Most common in severe infection: A.
naeslundii & A. meyeri.
Sulfur granules found in pus and
Listeria monocytogenes - SUPER MOTILE colonies of branching filamentous
CATEGORICAL 'tumbling motion' actinomyces.
TECHNICALLY INTRACELLULAR! Propionibacterium acnes- SMB
WHO: babies, old adults, immunocompromised PROSTHETIC DEVICES AND ACNE!
(alcoholics included) **osteomyelitis!!
Motile @ <30 C but NOT AT 37
THEREFORE IN CELLS USE EXPLOSIVE
MOVEMENT VIA ACTIN (virulence factor YAA)
Mothers SHOULD NOT eat soft cheese = L. mono
growth = VERTICAL TRANSMISSION
ALSO SUPER IMPORTANT = IT CAN CROSS
THE PLACENTA
OTHER reservoirs
soil, water, animals
VIRULENCE FACTORS:
LLO (listeriolysin O) -> pore forming, punches
phagolysosome and frees more bacteria
INTERLINS ** - helps entry
A&B: attach to cadherins in GIT, BBB and FETO/
PLACENTAL barriers
Actin motility - use host actin to move between cells
suppreses T cell
PATHOGENESIS
PATHOGENESIS
1) prevent oxidative burst and inhibit phag/lysosome fusion
EXPOSURE: inhalation of aerosols
2) resist lysosomal enzyme, ROS
AND CONTAMINATED WATER!
FACULATATIVELY INTRACELLULAR
LAB ID
(alveolar macs)
CULTURE
uptake via phag - prevent
LOWENSTEIN-JENSEN AGAR
phagosome-lysosome
OLEIC ACID -albumin broth
COMBINATION THERAPY
urinary ag EIA for diagnosis
FIRST LINE: Isoniazid***, RIFampin, STreptomycin, ethambutol
DRUG RESISTANCE
MAC
Advanced HIV infection and CD4+ count under 50 = predisposing factors
Consists of M. avum and M. intracellulare.
Weakly Gram (+ve) but due to mycolic acid it is strongly acid fast (aerobic
rods).
Causes disseminated infection; tissues and blood are filled with bacteria
(usually
localized to lung in immunocompetent).
Incidence = 20-30% of AIDS patients get MAC.
Symptoms: night sweats, weight loss, abdominal pain, diarrhea, fatigue, anemia.
ZOONOTIC SPECIES!
both categorized as gram - rods, all replicate in MACS!
TULAREMIA - YERSENIA species
BRUCELLA - Y. Pestis & Y. Enterolytica
Bartonella species
TULAREMIA - SMB, RESP, GI (typi)
B. abortus (cattle)
PATH: inhalation, ingestion, injection
B. suis - PIGS
minimum infectious dose <100 cells
B. canis - DOGS
infects RES with GRANULOMA
FORMATION
RESEVOIR
recovery = long lasting immunity
TRANSMISSION: skin breaks, mucus membranes, ACUTE ONSET: fever, chills, malaise
ulcero-glandular (injection --
killed via PASTEURIZATION
LEAST)
PATHOGENESIS
typhoidal (ingestion)
RES --> waves of bacteria released (= RECURRENT SERO: agglutinating abs 1:40 to 1:320
BACTEREMIA)
in 1-2 weeks
TREATMENT
STREPTOMYCIN/AMINGOGLYCOCIDE
LYMPHADENOPATHY/SPLENOMEGALY
CHRONIC
OUTDOOR OR
NOCTURNAL FEVER
ANIMAL
WEIGHT LOSS
ASSOCIATION
Depression
DIAGNOSIS
THERAPY
YERSENIA PESTIS
non spore forming
oxidase neg
faculatative
glucose fermenter
grows on standard media
PATH:
RAT FLEA (Xenophylla cheeps) --> gets Y. PESTIS from RAT -->
blocks GI of FLEA-- REGURGITATES infectious material --> org
reaches LN --> high temp = VIRULENCE FACTORS +
MULTIPLICATION --> LN SWELLS (BUBO) BACTEREMIA --> BARTONELLA SPECIES
Pulmonary infection --> TRANSMITTED FROM DROPLETS
(Pneumonic plague)
stupid cats
LN aspirate, blood smear if patient is septicemic, unculturable occurs in HIV positive patients
= DFA/PCR
SYMPTOMS: subcutaneous enlarging
TREATMENT
red papule (looks like cranberries)
no vaccine
PLAGUE AND HIV -- CCR5 mutation aka those that survived bubonic
also not susceptible to AIDS
YERSENIA Enterolytica - GI
INFLAMM. DIARRHEA!
CHILDREN 7 years of age as well as adults (cooler climates).
-1 C+40 C (Psychrotroph facultative psychrophile).
Likes to grow on refrigerated foods.
ST TOXIN - HEAT STABILE ENTEROTOXIN
INCREASE in cGMP
INTRACELLULAR - OBLIGATE
ANAEROBES
CANNOT REPRODUCE OUTSIDE CELL
RICKETTSIA species
Typhus
Spotted fever
Scrub typhus
Cox - Q fever
Chlamydia Species
trachomatis, LGV and non - UGI
pneumoniae - RESP
psittaci - ZOO
BACKGROUND
PROKARYOTIC
contains Peptidoglycan
Common features:
DIAGNOSIS: serologic
TREATMENT: TETRACYCLINE/CHLORAMPHENICOL,
within 1st week!
Reservoir -- MAN
GIEMSA STAINING!!
BRILL ZINNSER CARRIER STATE -- can be active years after
PEDICURES HUMANIS: likes 29-30 C, leave feverish and cooling SCRUB TYPHUS - rats -- chiggers -- man
corpse -- likes body odors and own excretion, avoids moisture, Orientia Tstsugamushi --RICKSETTIA LIKE,
prefers rough surfaces
chigger bites
only survive 10 days post infection -- uninfected only live 6 enlarged lymph, prostrate with pneumonia,
wks
cardiac/renal failure hemorrhage
secondary carrier: Sheep, cattle, goats
CONTROL: DDT.
RICKETTSIAL HEADACHE
DIAGNOSIS
SEROLOGIC (retrospective)
TREATMENT
TETRACYCLINE OR CHLORAMPHENICOL
BACKGROUND
TRANSMISISON
conjuctivitis (D-K)
gram -
endocervix, endometrium
anorectum
TESTING
USE NAAT
TREATMENT
AZITHROMYCIN 1 g orally
bird chlamydia -- FROM INHALATION OF DROPPINGS --> seeds the blood, other orgs
FEVER! CLINICAL
seeded in lung thru blood -- edema and thickening = MUCUS PLUGS = CYANOSIS
NONPrOdUCTIVE cough
Borrelia burgdorferi, B. garinii, and B. afzelii, = Lyme disease VERY INCREASED HIV TRANSMISSION
Treponema pallidum subspecies which cause treponematoses PRIMARY STAGE --> PAINLESS LESIONS
such as syphilis (hard, painless lesions)
NO Abs at this stage --> serological
1. Leptospirosis: Conjuctival RAT FEVER - L. testings not helpful
ENTERS: SKIN OR MUCOUS (splashing water in eyes, swallowing, wounds and LESIONS HAVE THING GREY CRUSH --
cuts on soil
> containsa lot of the org
FEMALES: chancre
1st phase (Leptospiremic phase): Host immune response > flu-like SECONDARY STAGE
symptoms, photophobia > resolves within a week as organism cleared. Maculopapular rash and SYSTEMIC
2nd phase (immune phase): Host immune response and rise in anti- INFECTION
leptospira IgM associated with mild or severe damage: flu like syndrome 2-8 weeks after ulcer
Weils disease (severe) > vasculitis with hemorrhagic complications, sandy patches of palms of hands, soles
kidney damage of feet, tongue
with renal failure, liver damage with jaundice. CONDYLOMATA LATA (NOT
CONDYLATA ACULUMLATA --
1st: BLOOD & CSF HPV)
late -- 2 +
septic abortion
SPECIES INFO
bites with meat allergy SADDLE NOSE
VARIABILITY
EGG HATCH (summer) --> LARVAE NEED BLOOD (FALL) --> COATING OF FIBRONECTIN PROTECTS AGAINST
Nymphs dormant in winter (blood meal before they can be adults phagocytosis
(spring - summer - most infectious) -- ADULTS LAY EGGS (summer- outer membrane proteins = ADHERENCE
fall)
DO NOT SURVIVE A LONG TIME - NO FOMITES
TICK IN VECTOR
Endarteritis & Granulomas
Boreal adhere to epith the midgut --> feeding = HIGH TEMP = PRIMARY: SKIN BREACH, Lesion helped but
VIRULENCE FACTORS --> orgs penetrate the gut and spread to bacteria moves via LN AND BLOOD
inflammatory response