INFECTIOUS AGENTS

(Dr. Lasaca)

Complement System:
1. Opsonization-C3b enhancement
2. Cytolysis- inv. of c5-c9
3. Inflammation- release of histamine

Vascular permeability

Viruses, Bacteria, and Parasites

*Normal Microbiota/Normal Flora:
1.
Eyes
2.
Nose and Throat
3.
Mouth
4.
Skin
5.
Large Intestine
6.
Urinary and Genital System

Bacterial Non-Granulomatous

# Of invading organisms
Portals of entry

*There should be a balance between the Internal and External

Factors!*
Microbial Agent

Inoculation

Decisive Period
(Int. Defense Mechanism)

=Mucous membranes
-Resp.tract
-GIT
-GU
-Conjunctiva
=Skin
=Parenteral rout

-Penetration/invasion
of host defenses
-Capsules
-Cell wall comp.
-enzymes
-siderophores
-Antigen variation
-cytoskeleton

- damage
to host cells/
cytopathic
effect

-direct

Adherence
Organism destroyed

Organism not destroyed

Res olve infection

(-) Rep

Latent/smoldering
Infection
(char. Lesions
can t be seen)

(+) Rep

Overt
Infection
(vis ible)

Non-Specific Res istance

Specific Res istance

(Response of the
Immune system)
3rd line
1. Specific
lymphocytes
(B&T cells)
2. Antibodies

1st line of defense

2nd line
1. Intact Skin
1. Phagocytic WBC
2. Mucous
2. Inflammation
Membranes and
3. Fever
secretions
4. Antimicrobial
3. Normal
substances
microbiota
Fever- res ponse of the human body to help us do away with the
offending organism
Phagocytosis:

Tissue Changes in Infection

Extracellular Organism
1. Release of locally acting enzymes
a. Staph: Coagulase (Fibrinogen)
2. Production of remotely acting toxins
-endotoxins
-exotoxins
-enterotoxins
Exotoxins- produced inside mostly of Gm (+) bacteria as part of
their growth and metabolis m
secreted or released following lysis into the surrounding
medium
Endotoxins- part of the outer portion of the cell wall.
Gm (-)
Enterotoxins- special exotoxins that act on intes tinal mucosal cells
V. Cholera
C. Perfringes
E. Coli
Shigella
NON-GRANULOMATOUS BACTERIAL INFECTIONS
GRAM (-) COCCI

Offending organis m

Engulfed by macrophages

Ingestion

Phagososme

Phagolysosome

Residual bodies

Release of materials

STAPHYLOCOCCUS
- Normal flora: Nasopharynx and skin
- Infective only following large dose inoculation
- Most often form SUPPURATIVE lesion with walled off
abscesses or spreading cellulitis
- Mild regional lymphandenitis
- S. Aureus Sepsis!FATAL! Emergency!
Furuncles (Boil)
Focal SUPERFICIAL suppurative inflammation of skin
beginning in a single hair follicle

Carbuncle:
deeper SUBCUTANEOUS suppurative spreading
laterally, generally involving skin of UPPER BACK or
NECK
Impetigo
Superficial infection, mostly in children, COLORED
CRUST, both by staph and strep
if strep Lymphangitic spread (Red Streaks)
Pneumonia
Generally destructive bronchopneumoniamay rupture
into pleura EMPYEMA
Endocarditis
Left or right sided
Most frequently destructive vegetative endocarditis
TOXIN RELATED DISEASES
1. Staph Food Poisoning
toxin in contaminated food
acute, self- limited, onset 1-6 hours after consumption
2. Toxic Shock Syndrome
sporadic
Related to infected tampons , intractable shock,
sometimes fatal
3. SSS
-

Staphylococcal Scalded Skin Syndrome

exfoliation
supepidermal blistering and exfoliation with minimal
inflammation
children

BACI LLUS:
Anthrax
B. Anthracis
Exotoxin hemorrhage, inflammation
Predominantly, a disease of sheep
In humans, forms a malignant pustule at entry site
(blisters, necrosis, edema, inflammation)
Pustular Lesion
CLOSTRI DIUM
soil
invade underconditions:
1.
Low Oxygen tension
2.
Previous tissue damage
3.
Poor phagocytosis
-poor immune system of patient
Clostridium tetani
Tetanospasmin Neurotoxin bloodstream binds to
peripheral nerve endings ascends to cell body in CNS,
all without causing no harm when it passes into the
pre-synaptic terminals of inhibitor spinal interneurons
production sympathetic manifestations
Clostridium Botulinum
Spores resist boiling
ingestion of toxin blood attaches to synaptic
vesicles of cholinergic nerves blocks release of
acetylcholine
descending paralysis
Found in:
1.
2.
3.
4.

Home-canned food
Less oxygen tension
Pickles
Sauerkraut

STREPTOCOCCUS:
2 Disease Patterns:
-Suppurative Inflammation
-Hypersensitivity disease
-Rheumatic Fever
-Glumerulonephritis
-Erythema Nodosum
1. Scarlet Fever
auto strep PHARYNGITIS + Rash caused by
Erythrogenic toxin
3-15 years old
Ras pberry/Strawberry tongue
Notorious ly associated with post streptococcal sequelae
2. Impetigo
3. Bronchopneumonia
Strep Pneumoniae
Most cases of Lobar Pneumonia (Polysaccharide
Caps ule)
bacterial meningitis
GRAM (+) BACILLI
1.
2.
3.

Bacillus
Clostridium
Corynebacterium

Clostridium Perfringes
Invasive infections:
Necrotizing cellulitis
Myonecrosis (gas gangrene)
produces gas bubbles in tissues (crepitations)
extensive necrosis of muscles
toxins induce active hemolysis
Clostridium difficili:
Ps eudomembranous colitis
(+) inflammatory exudates spewing out from crypts
seen: Clindamycin, Lincomycin, Cephalosporins
Antibiotic therapy

Alteration of colonic microflora

C. difficili exposure and colonization

Release of Toxin A&Toxin B

Colonic mucosal injury and inflammation

CORYNEBACTERIUM
Diphtheriae
-Inflammatory pseudomembrane
-Exotoxin

GRAM (-) COCCI

Neisseria
Meningococcal infection, clinical manifestations and associated
complications:
1.
Cerebrospinal meningitis
2.
Purulent conjunctivitis
3.
Pharyngitis
4.
Pericarditis, bacterial endocarditis, myocarditis
5.
Petechial rash
6.
Adrenal necrosis and hemorrhage
7.
Septicemia
8.
Osteomyelitis
9.
Gangrene
10. Septic arthritis
N.Meningitidis
2 Clinical Forms :
1. Meningococcemia
2. Acute bacterial meningitis
N. Gonorrheae
Gonorrheal urethritis
easily trans mitted sexually or by other contact
retrograde spread to other genitalia where a chronic
purulent inflammation is produced
if untreated:
peritoneum in females perihepatitis (Fitz-HughCurtis syndrome)
septic arthritis in both sexes
GRAM (-) COCCOBACILLI
1.
Haemophilus
2.
Bordetella
3.
Brucella
H. influenzae
primary pathogen for children below 1year old
Meningitis, URTI, epiglottitis, endocarditis , pneumonia
lesions are rich in neutrophils and fibrin giving a plastic
quality that resolves slowly and may scar
H.ducreyi
chancroid
BORDETELLA
B.Pertussis
whooping cough
highly communicable
usually a self limited childhood disease with violent
coughing paroxysms
Organism does NOT invade but produces exotoxin
Extensive coughing spells subcutaneous emphysema
or hypoxia
GRAM (-) BACI LLI
1.
Enterobacteria
2.
Es cherichia
3.
Klebsiella
4.
Proteus
5.
Salmonella
6.
Shigella
7.
Serratia

-Gas trointes tinal

tract

E.Coli
-

forms mass culture in human gut lumen

most common cause of uncomplicated UTIs
Also cause appendicitis, cholecystitis, diverticulitis
when it causes gram (-) bacteremia:endotoxin DIC &/
shock
entero invasive form: shigella like picture
toxigenic form: watery diarrhea, similar to cholera