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Gram Positive Bacteria

Cocci Bacilli
CAT+ - Staph Spore forming
CAT- -Strep ANAEROBE: Clostridium species
Aerobe: Bacillus Species

Non-spore forming,

CAT +

Non motiel - > Corneybacterium

Motile -> Listeria

CAT -

Erysipelothix, Lactobacillus, Acitinomyces, Norcardia

1.1 GRAM POSITIVE COCCI


first discerning test = CATALASE, tells if you have STAPH or STREP!
CATALASE TEST: H202 added and converted to H20 + O2 (bubbling reaction on culture)

STREP KEY WORDS


STAPH KEY WORDS
Alpha, beta, gama hemolysis
COAG +
Group A, Group B
MRSA, VISA
M and T proteins
BETA hemolysis
Pharyngitis, Scarlet fever
Exofilative toxin
TSS
BACITRACIN +

ASO
SSS Neonate Meningitis

Impetigo, furuncles

Rhematic fever
Penicillinase Acute glomerulonephritis

Strep TSS
Food Poisoning
Erysipelas, cellulitis

.COCCI.

A. STAPH SPECIES - CAT +

COAG test: clotting of rabbit plasma

+ = S. Aureus*

- = S. epidermidis, S. saphrophyticus

CHARACTERISTICS

cluster formation "bunch of grapes"

Facultative Anaerobe

Normal flora of skin

Virulence factors

Protein A:

binds the Fc portion of IgG molecules

INTERFERES WITH OPSONIZATION

Coagulase +: fibrin coating

resists phag. and localization of lesion!

Hemolysins, leukocidins: destroy RBCs and WBCs.

Hyaluronidase: breaks down CT - SPREAD


Assoc. SYSTEMS
Staphylokinase: Lyses formed clots
Lipase: breaks down fats.
SKIN

GI
HIV infections

descending UTI
STAPH AUREUS - CAT+, COAG+
(hem. spread)
CYTOTOXINS

1)ALPHA: chromosomal encoded, pore formation (like


Streptolysin o of strep)

2) Pyrogenic Exotoxin

Tcell mediated -> widespread cytokines

3) PVL (Panton Valentine Luek) - kills NEUTROPHILS

EXOTOXINS

4) ENTEROTOXIN! - FOOD POISON!

5) TOXIC SHOCK - TSST1

6) EXFOLIATINS - SSS in infants

SKIN INFECTIONS - SMB


1) TOXIN MEDIATED

EXOFOL TOXIN: Scalded Skin SYNDROME


Exotoxin release d/t wound or umbilicus cutting

Epidermis splits - DESMOSOMES - leads to DESQUAMATION

IN INFANTS
MINOR pressure = Nikolskys sign (skin separation)

BULLOUS IMPETIGO - more commonly S. Progenies but also


seen in strains that have exfoliation

TSST-1 - shock in 48 hours

Usually in young women, SUPERag - IL-1/TNF -->


HYPOTENSION and DESQUAM of palms and soles

only 5% women carry this vaginally Bulllous >.5 cm

diff from STREP "LIKE TSS" - deeper


2) Other SKIN INFECTIONS

a) CELLULITIS - **DIFF from Strep d/t Walling off and extension

b) Abscess - Neutrophils localize to site > form purulent

abscesses > skin/ subcutaneous infections or pneumonia

bacteria may invade and reach bloodstream.


c) FURUNCLE AND CARBUNCLES

further FURUNCULOSIS d/t DELAYED HS rxn -->

COMPLICATED by CGD AND diabetes


d) STYE

OTHER IMPLICATIONS

GI - ENTEROTOXIN BACTERIAL CONJUNCTIVITIS (TISSUES)

Food POISONING!/preformed toxin


DESCENDING UTI - SEPTICEMIA due to blood

ST TOXIN but NO stim of ADENYLATE CYCLASE! spread

heat stable toxin!


ACUTE ENDOCARDITIS IN DRUG USERS!

found in the nares of the nose


2 + Blood samples, treat with methicillin

produces 8 ENTERoTOXINS (A, B, C1, C2, C3, D, E, H)


ABSCESS - lung, brain, etc
Associated with bacterial pneumonias

A & D the most typical

works on the gut receptors (vagus and sympathetic increased susceptibility in HIV patients

nerves) - VAGUS = NEURO (vomiting), SYMP

(diarrhea)

WHEN: Symptoms start within 6 hrs

recovery in about 1-2 days (SELF LIMITING)


more popular in SUMMER!, second most = holidays

FOOD: Cream filled pastries, meat, bakery, dairy produce,


ANYTHING WITH MAYO!!!

***POOR HANDLING OF FOOD!


DIFF DX: B. CEREUS, similar action


STAPH AUREUS ID

NONSELECTIVE: Bood Agar (Beta)

**BAIRD PARKER -- SELECTIVE


LiCL + Tellurite

Egg yolk & pyruvate


reduction of tellurite --> SHINY JET BLACK

COLONIES , surrounded by learning zone


CONFIRMATION TEST: COAGULASE TEST


ANTIBX/TREATMENT - problem in hospitals!!!

MRSA, VRSA, VISA, hVISA exhibit antibiotic

resistance; VISA and hVISA hard to detect (below lab

detection level).

Many strains resistant to Penicillin G; VRSA strains

handled with most caution.


MRSA is typically HAI; treat community-acquired

MRSA with clindamycin).- this one has PVL TOXIN!


COAGULASE NEGATIVE STAPH

S. Epidermidis, S. SAPROPHYTICUS, S. lugdunesis


S. Epidermidis

SMB

BIOFILM PRODUCER!

seen in artificial HEART VALVES and CSF shunts


S. Sapro -

UGI
UTI IN SEXUALLY ACTIVE FEMALES!

occurs mostly in the summer


WHOLE GENOME SEQUENCING


due to novel cell wall-anchored adhesin


redundant uro-adaptive transport systems

urease

S. Lugdunesis

SMB

A LOT like S. Aureus, can produce skin and soft tissue infections

B. STREP SPECIES - CAT -


divided in 7 groups based on 16rRNA --
only two we care about here are:
1) PYOGENIC GROUP: S.
pyogenes, S. agalactiae
2) Mitts group: S. pneumoniae, S.
mitis
Hemolysis
A-hemolytic (H202 production --
converts haemoglobin to
metamoglobin = GREEN!)
S. pneumoniae, S mitis
B- hemolytic (HAEMOLYSIN clear)
GROUP A: S. progenies
GROUP B: S. agalactiae
NON-hemolytic = Enterococcus

ALPHA HEMOLYTIC
S. pneumonaiea (opt senstive, quelling +)

SYNDROME: pneumonia, sinusitis, OTITIS media, MENINGITIS!

**NUMBER ONE CAUSE OF CAP, via droplets


ADULTS: primary cuase is bacterial


STREP ASSOCIATED CLINICAL


infants and children: RSV, HPIV, flu A & B

LAB ID
STREP PNEUMONIA

LANCET SHAPED IN PAIRS


LOBAR pneumonia - healthy persons
ALPHA HEMOLYTIC!!!!
exposed to cold, exhaustion

OPTOCHIN SENSITIVE, BACITRACIN RESISTANT!!!


early stage = exudate with fibrin, RBC, PMN


SPREAD via pores of KOHN

PATHOGENESIS:
RED HEPATIZATION: exudate w/ RBCs fibrin,
CARRIAGE: throat/nasopharynx
**VIRULENCE FACTORS PMNs, becomes SOLID

CAPSULE** CROSS REACTING Abs deposited on normal


18 SEROTYPES (prevents complement interaction - C3b) tissues [Rheumatic fever]

IgA protease Strep infection (lag 2-3 weeks) --> fever,


**Pneumolysin polyarthritis, carditis, chorea, erythema
pore forming = NEUROTOXIN (leads to apoptosis)
Hydrogen peroxide (ACCNE) --> Abs to M protein of bacteria
no catalase so build up = cell death cross react w/ tissue glycoprotein in joints,
Other Facts Re: Virulence: heart and skin

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!

strep sore throat (lag period 1-4) --> fever,



oliguria, hematuria --> INCREASE IN BUN,

SUBACUTE ENDO!
CREATINE, DECREASE in GFR,
VIRIDANS - (OPTOCHIN R) TREAT w/ Pen. G
**for pts getting HYPERTENSION --> Antibodies/Ag Immune
S. Mutans - dental caries
dental work = complexes deposited in BM of glomeruli-->
transient bacteremia
penicillin prophylaxis complment = INFLAMMATION

***ENDOCARDITIS, Subacute

S. Bovs - associated with colon cancer, Endocarditis assoc

with CCa

BETA HEMOLYTIC

GROUP A

S. PYOGENES (normal microflora, nasopharynx)


GROUP A B Hemolytic STREP -- inducer of puss, leukocidin

production

short chains of cocci

appearance on BA
B-hemolytic
small colonies without pigment
**BACITRACIN SENSITIVE, OPTOCHIN
RESISTANT!
Pen. Sus

VIRULENCE FACTORS

Streptokinase: converts plasminogen to plasmin > fibrinolysis.


Scarlet Fever: (complication of S.
Streptolysin O: PORE FORMING, O2 labile
pyogenes pharyngitis) > systemic
responsible for elevated ASO titer release of pyogenic exotoxins A, B,
Streptolysin S: "stable" 02
C > feverish sandpaper rash
M protein: resists phagocytosis. (see acute rheumatic fever)
(begins on trunk and spreads
hair like pilli on surface
reponsible for the type II HS rxn
outwards), Strawberry tongue within
first two days, desquamation of palms
F protein: helps with binding
and soles after rash subsides.
Hyaluronidase: breaks down connective

DNase: digests DNA.


TOXINS PRODUCED

Group A toxin aka Pyogenic EXOtoxin


carried on phage

responsible for rashes and scarlett fever


MANIFESTATIONS:

RESP: Pharyngitis transmitted human-to-human via respiratory


droplets or food > adhere to pharyngeal epithelium via pili and

colonize > inflammation > sore throat, enlarged cervical lymph


Toxic Shock Syndrome: (complication of S.
nodes > spontaneous recovery, or may lead to:
Bacterial spread > bacteremia, meningitis, otitis.
pyogenes skin infection) > systemic release of
Toxin release > scarlet fever, TSS.
pyrogenic exotoxin A (superantigen) >
Anti-streptococcal Ab reactions > glomerulonephritis (10 days polyclonal activation of T cells > acute fever,
post infection), rheumatic fever.

shock, multi-organ failure.
SMB: Skin infections: Trauma inoculates bacteria into skin >

bacteria colonize > inflammation > pustular lesions and

honeycomb-like crusts (impetigo) at site of inoculation > deeper


infection results in erysipelas, cellulitis > spontaneous recover,
or may lead to anti-strep Ab reactions.
Pain, fever and lymphadenopathy come with the latter
Erysipelas usually from shaving!

TREATMENT: GENERAL, PEN G

FOR IMPETIGO: Cephalosporins!

ERYSPELAS: Topical,

superficial lymph
CELLULITIS: accompanied

with fever, bacteria, chills

GROUP B

S. Agalactiae -

GROUP B, BACITRACIN RESISTANT!

normal flora of the vagina - vertical transmission

NEONATAL MENINGITIS, and pneumonia


GRAM POSITIVE: BACILLI


1.2 NONE SPORE FORMING

1.1 SPORE FORMING


CATALASE +

ANAEROBE -> CLOSTRIDIUM SPECIES


Nonmotile -> Corneybacterium

C. Dicile
Motile -> Listeria Monocytones

C. Botulinum
CATALASE -

C. perfringens
Erysipelothix

C. tetani
Lactobacillus

AEROBE -> Bacillus Species


Actinomyces

B. Anthracis
Nocardia

B. Cereus
Propionibacterium

1.1 SPORE FORMING: CLOSTRIDIUM SPECIES

SYSTEMS
CLOSTRIDIUM SPECIES - GI - all three

ANAEROBIC SKIN

C. Botulinum - FOOD POISONING; GI

ENTERIC = Vomits, TOXIN: A-B NT

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

8 types of neurotoxin (A,B,C1,C2,D,E,F,G) proteins. Toxin A is


potent (108 lethal). US frequent isolate type A, then B and E.
Europe frequently isolates type B (A rare).
almost all type E.

Adult botulism: Heat-labile toxin is released in anaerobic


environment, especially in canned foods > ingestion of
contaminated food > neurotoxin quickly enters vascular
system and spreads to peripheral cholinergic nerve
terminals Diff Dx:
(12-36 hours) LONGEST FOOD POISON INCUBATION MG: Descending paralysis, fatigue w/ exercise
> blocks acetylcholine release at: GB: ascending paralysis with high CSF protein
Cranial nerves > diplopia, dysarthria, dysphagia.

NMJ = DESCENDING PARALYSIS (~MG)

Postganglionic parasympathetic nerve endings;


peripheral ganglia > dizziness, dry throat, ptosis.
VOMITING AND DIARRHEA!
NO FEVER because bacteria do not invade.

Infant botulism: NOT FOOD POISONING, types A&B


Spores in honey > spores germinate in large intestine > C. Difficle - GI
release toxin > toxin slowly absorbed (over days) > blocks
acetylcholine release > constipation, flaccid paralysis (floppy CAUSED BY ABx: clindamycin and Methotrexate
baby syndrome) => good prognosis with supportive therapy. normal flora usually occupy BINDING SITES
Lethargy/ Suck and gag reflex diminish - dysphagia becomes
evident as drooling. Head control lost, then flaccid. Toxin A: ENTERTOXIN
TREATMENT: HEPTAVALENT ANTITOXIN, BIG-IV - increased fluid secretion = diarrhea
Toxin B: CYTOTOXIN
- decreases cellular protein synthesis
disrupts microfilament system of cells =>
C. Perfringens: GI and SKIN cytotoxic to epithelial cells >
Non motile (only C species) pseudomembrane formation.
encapsulated SYMPTOMS: FEVER! Ab pain, mucus and pus
Toxins Produced TREATMENT: VANCO!
Alpha: Necrotic
Theta: pore formation - toxic to capillaries/

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]

2) Type A food borne infection - TYPE A

improperly cooke MEAT AND MEAT PRODUCTS


LIKE GRAVY!

PATHOGENSIS: 10^6-10^8 --> sits on meat --> meat


survives cooking/germination while resting --> CPE
produced in SMALL INTESTINE! = watery diarrhea

inc: up to one day, NO FEVER or VOMITING


Diff dx: non spore former + bacilli: Acitinomycetes and


not killed by cooking Nocardia

BACILLUS SPECIES - AEROBIC

B. ANTHRACIS - GI, SKIN, RESP

B. CEREUS - GI

B. ANTHRACIS - SKIN, GI, RESP


ZOONOTIC! LF!!! - necrosis =
CHARACTERISTIC
ESCHAR
BOX CAR RODS

NON MOTILE/NON HEMOLYTICS

CAPSULE, GLUTAMYL POLYPEPTIDE: amount of capsule correlates


directly with virulence

VIRULENCE (LF, EF, PA)


lethal factor - hydrolysis of kinases


tissue necrosis, tissue swelling (increased distribution of

lethal factor)

protective Ag
KEY WORDS: Farm,

PA+EF = EDEMA TOXIN


Hides, Soil, LT, ET

PA+ LF = LETHAL TOXIN


THREE GENES: CapA, B, C on plasmid

EDEMA TOXIN = cAMP allows fluid in tissue

LETHAL TOXIN: macrophages release TNFa, IL1 and cytokines

-- both LF/EF inhibit innate immune

CLINICAL MANIFESTATIONS: Cutaneous (least life threatening), GI,


Pulmonary (highest mortality)

1) CUTANEOUS - MOST COMMON - ULCER!


begins at primary site as PAPULE, produces black NECROTIC ulcer


(eschar)

edema, redness

INCUBATION: 1-12 days

FATALITY - w/o antibiotic treatment -- 20%, WITH -- 1%

2) GI

AB distress with bloody vomiting/diarrhea, FEVER and SEPTICEMIA

OROPHARYNGEAL ULCERS and cervical adenopathy

Develops after ingestion of CONTAMINATED poorly cooked meat

INCUBATION: 1-7days

3) PULMONARY -- INHALATION ANTRHAX - WOOL SORTERS DISEASE

viral/flu-like illness fatigue, dyspnea, MENINGITIS IN 50% of patients

INCUBATION 1-7 days

WITHOUT treatment - 97%, with 75%

DIAGNOSIS & MANAGEMENT


culture of lesions/biopsy, stains PCR
blood cultures

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

can cause suocation


DEEP SKIN ISSUE!
**EXOTOXIN: genes acquired thru lysogenic TREATMENT: PEN!!
conversion (PHAGE)

responsible for local and systemic symptoms

PSEUDOMEMBRANE --> damage to organs

TESTS: ELEK, TINSDALE Non MOTILE

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

only Gram + with endotoxin,


TUMBLING!
INTRACELLULAR ORGANISMS!
FACULATATIVE INTRACELLULAR
can reproduce inside OR outside of cell
MYCOBACTERIUM SPECIES
Legionella
BRUCELLA - ZOO
Tularemia - ZOO Legionella Pneumoniae
YERSINIA - ZOO
Bartonella - ZOO
Nocardia GRAM - RODS- ONE SINGLE POLAR
FLAGELLA
MYCO SPECIES! SYNDROME: Legionnaires disease
(PNEUMONIA!), pontiac fever
MYCO. PNEUMONIAE - TB SEROTYPES BASED ON O Ag, no
RESP, HIV
capsule
PEPTIDOGLYCAN: similar to Gram + -- NAM/NAG cross linked with NAM/
NAG w/ D-mesodiaminopimelyl
can survive @ 50 C ~30mins ---
LIPID RICH - mycelia acids
WITHSTANDS chemical
resistant to detergents, hydrophobic
**HIV: #1 treatment
LAM - similar to O antigen LPS
coinfection! found in water environments
activates cytokine

suppreses T cell

"TWIN EPIDEMIC" both natural/artificial


inhibits IFN activation of macrophages

PATHOGENESIS
PATHOGENESIS
1) prevent oxidative burst and inhibit phag/lysosome fusion
EXPOSURE: inhalation of aerosols
2) resist lysosomal enzyme, ROS
AND CONTAMINATED WATER!

CELL WALL LIPIDS, LAM, secretion of superoxide disputes

3) iron acquisition thru sidephore --> myobactins

FACULATATIVELY INTRACELLULAR
LAB ID
(alveolar macs)

CULTURE
uptake via phag - prevent
LOWENSTEIN-JENSEN AGAR
phagosome-lysosome
OLEIC ACID -albumin broth

ZIEHL NEELSEN/ACID FAST staining


PREVENTION
LAB ID
prophylatic antimycotic after exposure
BYCE

COMBINATION THERAPY
urinary ag EIA for diagnosis
FIRST LINE: Isoniazid***, RIFampin, STreptomycin, ethambutol

**BCG vaccination -- live attenuated M. bovid strain (false positive test)

DRUG RESISTANCE

MDR-TB: resistant to ISONIAZID and RIFAMPIN

XDR-TB: MDR + resistant to fluoroquinolone plus one of three injectable


drugs

Amikacin, Capreomycin, kanamycin

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.

MYCOPLASM UREA - UGI


Among smallest, lack a cell wall, STEROLS
Symptomless (or symptoms: discharge, burning, urinary frequency, and pain
Mycoplasma Gentalium: Genitourinary tract > NGU, PID.
Ureaplasma Urealyticum: Respiratory and Genitourinary tract > NGU,
pyelonephritis, spontaneous
abortion, premature birth.
DETECTION: NAAT!

INTRACELLULAR FACULATATIVE ANAEROBES cont'd

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)

BRUCELLA - DIRECT CONTACT AND FRANCISELLA TULARENSIS


INGESTION!
GRAM NEG. COCCOBACILLUS, FACULATATIVE,
INTRACELLULAR but labeled as gram - coco bacilli
non spore forming

FASTIDIOUS, will NOT grow on blood -- need


HAVE 2 chromosomes of UNEQUAL SIZE, some have SULFHYDRYL components (cyst-glucose)
small capsule, strict AEROBES, FASTIDIOUS, grown with CYSTEIN-GLUCOSE BLOOD AGAR
INTRACELLULAR!!!, need complex artificial media (5% (AEROBIC)

CO2 for growth in vitro), slow growing.


slow growing -- needs 2-10 days for visible growth

EPI: small wild animals (RABBITS,


4 CLINICAL TYPES IN HUMANS
ASSOCIATED WITH SQUIERRELS) -- TICKS and deer flies

B. melitensis (goats sheep camels)


DIARY CONSUMP! NA, CANADA, MEXICO

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

venereal disease of farm animals


CLINICAL

direct occupational contact = BUTCHERS, VETS


INCUBATION: 2-5 days

TRANSMISSION: skin breaks, mucus membranes, ACUTE ONSET: fever, chills, malaise

aerosols, ingestion of infectious dairy products -- DEPENDS ON SITE OF INJECTION

ulcero-glandular (injection --
killed via PASTEURIZATION
LEAST)

PATHOGENESIS
typhoidal (ingestion)

penetrate skin/mucosal --> carried by LYMPHATICS pneumonia (inhalation: greatest


BY PMNS --> multiply in MACs (PREVENT PHAGO- mortality)

ALL BECOME SYSTEMIC

LYSO FUSION) --> HUMORAL IMMUNITY HAS NO


DIAGNOSIS

EFFECT, T CELL RESPONSE IS THE ONLY rarely suspected

CONTROL, FAILURE OF T CELLS = granulomas in DIRECT FLUORESCENT ab

RES --> waves of bacteria released (= RECURRENT SERO: agglutinating abs 1:40 to 1:320
BACTEREMIA)
in 1-2 weeks

TREATMENT

ACUTE: INCUBATION= 7 to 21 days, flu like

STREPTOMYCIN/AMINGOGLYCOCIDE

DRENCHING SWEAT, high FEVER,


MUSCULO SKELETAL PAIN, SCROTAL

B. MELITENESIS (GOAT, SHEEP) MOST ULCERS!!!


SERIOUS, B. suis = ABSCESS FORMATION

LYMPHADENOPATHY/SPLENOMEGALY

CHRONIC
OUTDOOR OR
NOCTURNAL FEVER
ANIMAL
WEIGHT LOSS
ASSOCIATION
Depression

DIAGNOSIS

rise in titer to 1:640 - acute disease

ISOLATION AND CULTURE = DEFINITIVE

DIFF. DIAG: must incubate in CO2 for B. abortus

prolonged incubation for blood cultures (2-4 weeks)

THERAPY

CHEMO DOES NOT GIVE RAPID RESULTS

TETRACYLINE = main ABx


steptomycin, gentamicin, RIF used as secondary
YERSENIA SPECIES
Y. Pestis - ZOO
Y. Enterolytica - GI

YERSENIA PESTIS
non spore forming

oxidase neg

faculatative

glucose fermenter
grows on standard media

polysaccharide capsule = VIRULENT!

WESTERN USA! - CALI, etc!

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

BARTONELLA HENSELAE -- catch


ACUTE STAGE
scratch
BUBONIC (4-7) days
symptoms: papule or pustule -- heals
swollen painful LNs (inguinal!), fever, imcrohemmoraghes spontaneously but 2-3 weeks later
in the face
LYMPHADENoPATHY for 2-4 months

PNEUMONIC 18-36 hours


ID WARTHIN STARRY SKY

VIOLENT PNEUMONIA - fatal


BACILLARY ANGIOMATOSIS (R.
DIAG: ID = WAYSON STAIN!
HEnselae) - HIV

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

DOXY (100) AND CIPRO (500) - 1 week.


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

Transmitted in raw milk or fecal-oral route > localizes in


terminal ileum > secretes heat- stable enterotoxin (similar to
E. coli ST toxin) to give diarrhea > ulcerates colon and
produces dysentery-like symptoms. HIV: 1st appears as purplish to bright red
skin patches, often resembling Kaposis
go to mesenteric lymph nodes cause mesenteric adenitis. sarcoma
**MIMICS APENDCITIS!!!
period 3-7 days; duration 2-3 weeks (or longer)
can have reactive arthritis!
TREAT: oxytetracycline or doxycycline
ID: grows on MacCONKEY - pinpoint colonies at 48 hours

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

I. RICKETTSIA SPECIES - ZOONOTIC!


RICKSETTIA - GRAM (-), coccoid - INTRACELLULAR

BACKGROUND

PROKARYOTIC

contains Peptidoglycan

Oxidize Glutamic and Citric acids, Not glucose

Leaky cell membrane --> ATP exchanged for ADP in both


directions

Common features:

primary infection =vascular epithelium -> leakage into


surrounding tissues

CLINICAL: high fever, headaches, spread of lesions--> RASH.

R. RICKETTSI - DOG TICK


ROCKY MOUNTAIN SPOTTED FEVER

INCUBATION: 2-6 days

ACUTE SYMPTOMS: fever, headache, toxicity, mental


confusion, myalgia, KOPLICS LIKE MEASLES!

RASH: appears on wrists or ankles and spreads inward to


trunk -- covers the hands and soles of the feet

DIC, THROMBOCYTOPENIA, ENCEPHALITIS,


VASCULAR COLLAPSE

DIAGNOSIS: serologic

TREATMENT: TETRACYCLINE/CHLORAMPHENICOL,
within 1st week!

CAN be confused with human echilosis


R. PROWAZEKII

Reservoir -- MAN
GIEMSA STAINING!!
BRILL ZINNSER CARRIER STATE -- can be active years after

Transmission: human flea, PEDICULUS HUMANIS

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

INFECTION = FATAL TO VECTOR


transmitted by mites

progeny Rickettsiae are released into fecal stream


incubation: 9 days, RASH @5th/7th day

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.

TYPHUS -- R. prowazekii, R. typhi


7-14 days post bite

RICKETTSIAL HEADACHE

EXANTHEMA -- on trunk then to extremities

COMPLICATIONS: myocarditis, vascular collapse, CNS


dysfunction

DIAGNOSIS

SEROLOGIC (retrospective)

therapy started based o symptoms

TREATMENT

TETRACYCLINE OR CHLORAMPHENICOL

PROGNOSIS: delay of therapy = increased fatality


COXIELLA BURNETTI -- "Q fever" ( inhalation!)
ZOO!

BACKGROUND

morphology similar to RICKETSSIA / dierent DNA SEQ

multiple in host cell phagolysosome -- likes low PH

highly resistant to drying

exists in dusts at temps as high as 40 C

TRANSMISISON

mostly via dusts

PHASE I: in tact LPS (VERY VIRULENT) -- IgM for


both
PHASE II: truncated LPS

INCUBATION: 7-21 days

CLINICAL: fever chills and headache, patchy interstitial


pneumonia, NO RASH

COMPLICATIONS: could present with endocarditis or


encephalitis (rare)

DIAGNOSIS: SEROLOGICAL, increase in TITERS //


complement or IF
REPLICATION/PATH
TREATMENT: usually supportive care (can use tetra tho ) - EBS attach to microvilli --> stay in the
cytoplasmic phagosome --> EB outer
DOXY membrane inhibits fusion to lysosomes (no
killing of chlamydia)

CHLAMYDIA SPECIES 6-8 hours: EBS become


METABOLICALLY ACTIVE Rbs

18-24: RBs become smaller Ebs


again -- ruptures cell
C. TRICH

dier in major outer membrane proteins and associated with di


diseases

AGENT OF TRACHOMA (A, B, Ba, C)

conjuctivitis (D-K)

infant pneumonia (D-K)


OTHER
urogenital disease (D-K)
COMPLICATIONS:
LV (LGV 1-2, -3)
BACTERIAL
Complications in women CONJUNCTIVIS!
INFERTILITY
LGV
ECTOPIC PREG
Reiters Syndrome --
CHRONIC PELVIC PAIN

assoc. with arthritis


CHARACTERISTICS

gram -

INFECTIOUS FORM --> EB


Noninfectious --> RETICULATE BODIES
NOT VISIBLE ON GRAM STAIN
PATHOGENESIS

Receptors for EBs

mucous membranes of the urethra

endocervix, endometrium

anorectum

respiratore tract and conjunctivae

TESTING

NEED A SWAB NOT EXUDATE --

USE NAAT

TREATMENT

AZITHROMYCIN 1 g orally

doxycycline 100 mg orally 2X day for 7 days

screening and treatment

bird chlamydia -- FROM INHALATION OF DROPPINGS --> seeds the blood, other orgs

C. psittaci BACKGROUND: no peptidoglycan wall, LPS with with toxicity


PARROT MOMP is a surface cell wall component unique to each

OMP IS COMMON TO ALL

FEVER! CLINICAL

seeded in lung thru blood -- edema and thickening = MUCUS PLUGS = CYANOSIS

INCUBATION 5-14 days

NONPrOdUCTIVE cough

CNS - convulsions, coma, encephalitis, death

GI symptoms - vomiting diarrhea

***hepatomegaly, splenomagaly and keratoconjunctivitis

DIAGNOSIS: SEROLOGY, patient isolation and abs


3. TREPONEMA PALLIDUM - SYPHILLIS
SPIROCHETES
Leptospira species - interrogens easily curable in the first and second stages

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

interrogans NEED A DARKFIELD MICROSCOPE -->


HUMANS ARE DEAD END HOST - infection asymptomatic in the animal host
need EXUDATE

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

Anicteric leptospirosis (mild) > aseptic meningitis. MOST INFECTIOUS STATE!!!!

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)

2nd: URINE more wet and mucous

TERTIARY (15-20 years pi)

Four syndromes (after 1-2 week incubation):


diuse chronic inflammation

Bacteremia: Flu-like, diarrhea, and vomiting; conjunctival congestion.


Meningitis: Aseptic meningitis. neurosyphylis ---> DEMENTIA -->
Icteric: Fever, hemorrhages, hepatic and renal impairment. gummatous, a hypersensitive
Pulmonary: ARDS granulomatous reaction

DIAG: INCREASE IN PMNS & Liver enzymes, DECREASE IN

PLATELETS! CONGENITAL SYPHILIS

early before 2 years

late -- 2 +

CAN CROSS UTERINE and PLACENTAL


2. Borrelia Bugdorferi - LYMES DISEASE! MEMBRANE

septic abortion

IXODES SP. -- LYMES DISEASE


ALPHA-GAL = connects tick
clinical of late stage: STROMAL GAZE, keratitis

SPECIES INFO
bites with meat allergy SADDLE NOSE

outer membrane proteins encoded on plasmids = ANTIGENIC


pointing of teeth

VARIABILITY

PATHOGENESIS - nymphs feed in the summer mostly!


(HEAT BASED ACTIVATION)!


PATHOGENESIS

COMPLETE CYCLE takes 2 calendar years!


hyluronidase = SPREAD

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

SLOW REPLICATION, FASTIDIOUS

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

SALIVARY GLANDS OF THE TICK --> INJECTED INTO SKIN of host


SECONDARY: evasion of immune system,

inflammatory response

DISEASE STAGES ANALOGOUS TO SYPHILIS!!! TERTIARY: diuse chronic

1 - ECM -- bullseye ***DIAGNOSIS

2 - secondary annular skin lesions (exanthema) -- palms and soles


RAPID WITH DARK FIELD EXAMINATION OF
CNS, cardio involvment
EXUDATE -- highly sensitive

3 - ACA (acrodermatitis Chronicum Atrophicans)


NON TREP TESTS (NON SPECIFIC
LOTS OF CNS symptoms, cardiomyopathy
cardiolipins) -- DISEASE STATE!

a lot of false positives - pregnant, drug


DIAG: early -- BLOOD SMEAR, LATE, ELISA/IFA
WESTERN BLOT abuser, autoimmune

TREATMENT: DOXY/AMOX: EARLY not recommended as the first test


MORE SPECIFIC
ANYMORE

CEFTRIAXONE or CEFO for late! BUT LESS TREPONEMAL -- MONITORING TREATMENT,


RELIABLE ANTIBODIES

will come up if person is not having


symptoms

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