Bacterial Diseases

Gram-positiveGram-negative

Rickettsias, Chlamydias, Spirochetes and Vibrios

Bacterial Diseases Classified by:

AirborneUpperLower

FoodborneWaterborneSoilborneArthropodbornePhysical Contact

STDContact Animal

Or by…..

Physiological properties:Catalase

Hydrogen peroxide water

OxidaseWater hydrogen peroxide

PeroxidaseBreakdown peroxidase (by-products that cause

tissue damage)

Or, by……..

Gram-positiveGram-negativeRickettsias, Chlamydias, Spirochetes and

Vibrios

Gram-positive bacteria

Staphylococcus aureusCapsule!grows in large, round,

opaque coloniesoptimum temperature

37oCfacultative anaerobewithstands high salt,

extremes in pH, & high temperatures

produces many virulence factors

Enzymes of S. aureusCoagulase

coagulates plasma and blood

produced by 97% of human isolates

Hyaluronidasepromotes invasion

Staphylokinasedigests blood clots

Dnasedigests DNA

Lipaseshelps bacteria colonize oily

skin

Penicillinase inactivates penicillin

Toxins of S. aureus

hemolysins lyse RBCs

Leukocidindamages cell membranes

Enterotoxinsact in the gastrointestinal tract

exfoliative toxinseparates epidermal layers

toxic shock syndrome toxin (TSST)

Epidemiology and PathogenesisPresent in most environments frequented by

humansReadily isolated from fomitesCarriage rate for healthy adults is 20-60%

mostly in anterior nares, skin, nasopharynx, intestine

Predisposition to infection include: poor hygiene and nutrition, tissue injury, preexisting

primary infection, diabetes, immunodeficiency

Increase in community acquired methicillin resistance MRSA

Staphylococcal Disease - 1Localized cutaneous infections – invade skin through

wounds, follicles, or glands folliculitis

superficial inflammation of hair follicleusually resolved with no complications but can progress

furuncle Boilinflammation of hair follicle or sebaceous gland progresses into abscess

or pustule carbuncle

larger and deeper lesion created by aggregation and interconnection of a cluster of furuncles

impetigo bubble-like swellings that can break and peel awaymost common in newborns

Staphylococcal Disease - 2

Systemic infections osteomyelitis

infection is established in the metaphysis

abscess formsbacteremia

primary origin is bacteria from another infected site or medical devices

endocarditis possible

Staphylococcal Disease - 3Toxigenic disease

food intoxicationingestion of heat stable

enterotoxinsgastrointestinal distress

staphylococcal scalded skin syndrome toxin induces bright red flush,

blisters, then desquamation of the epidermis

toxic shock syndrome toxemia leading to shock and

organ failure

Other Staphylococci

S. epidermidis lives on skin & mucous

membranesendocarditis, bacteremia, UTI

S. hominis lives around apocrine sweat

glandsS. capitis

live on scalp, face, external ear

S. saprophyticus infrequently lives on skin,

intestine, vagina; UTI

Streptococci

Gram-positive spherical/ovoid cocci arranged in long chainsNon-spore-forming, nonmotileCan form capsules & slime layersFacultative anaerobesSensitive to drying, heat & disinfectants 25 species

Streptococci

Lancefield classification system based on cell wall Ag 17 groups (A,B,C,….)

Another classification system is based on hemolysis reactions -hemolysis

A,B,C,G & some D strains –hemolysis

S. pneumoniae & others collectively called viridans

γ-hemolysis Enterococcus faecalis does not induce hemolysis

StreptococciSkin infections Impetigo (pyoderma)

superficial lesions that break and form highly contagious crust

often occurs in epidemics in school children

associated with insect bites, poor hygiene, and crowded living conditions

Erysipelas pathogen enters through a break in the

skin eventually spreads to the dermis and

subcutaneous tissues can remain superficial or become

systemic

Throat infections Streptococcal pharyngitis

strep throat

-hemolytic S. pyogenes

Most serious streptococcal pathogen

Inhabits throat, nasopharynx, occasionally skin

Produces C-carbohydrates, M-protein (fimbrae), streptokinase, hyaluronidase, DNase, hemolysins

S. pyogenes

GASProduces toxinsHumans only reservoirTransmission

contact, droplets, food, fomites

Skin infections pyoderma, impetigo,

erysipelas

Systemic infections strep throat, pharyngitis,

scarlet fever

S. pyogenes

Causes streptococcal pharyngitis Strep throat enters the upper

respiratory tract through respiratory droplets

Some patients with strep throat may develop scarlet feverexhibiting a rash caused

by erythrogenic exotoxins

S. pyogenes

Rheumatic fever serious complication

affecting the joints and heart

causes permanent heart damage called rheumatic heart disease

Acute glomerulonephritus rare inflammatory

response to M proteins may lead to renal damage

Group B: S. agalactiae

Regularly resides in human vagina, pharynx & large intestine

wound and skin infections & endocarditis in debilitated people

can be transferred to infant during delivery & cause severe infectionMost prevalent cause of neonatal pneumonia, sepsis, &

meningitisTargets infants without Ab, and mothers that do not

provide passive immunityPregnant women should be screened & treated

“Typical” Pneumonia Can Be Caused by Several Bacteria:

80% of “typical” pneumonia cases are caused by Streptococcus pneumoniae

Others: Haemophilus

influenzaeStaphylococcus aureusKlebsiella pneumoniae

Streptococcus pneumoniae

Small, lancet-shaped cells arranged in pairs and short chains

Culture requires blood or chocolate agar

Growth improved by 5-10% CO2

Lack catalase & peroxidases cultures die in O2

S. pneumoniae

All pathogenic strains form large capsules major virulence factor

Vaccine available for high risk people

S. Pneumoniae Epidemiology

5-50% of all people carry it as normal flora in pharynx

Does not survive long outside of its habitatPneumonia occurs when cells are

aspirated into the lungs of susceptible individuals

Pneumococci multiply induce inflammatory response

Traditionally treated with penicillin G or VIncreased drug resistance

Cultivation and Diagnosis

Gram stain of specimen presumptive identification

α hemolyticQuellung test or capsular swelling

reaction

Bacillus

gram-positiveendospore-formingmotile rodsmostly saprobic

primary habitat is soilversatile in degrading complex macromoleculessource of antibiotics2 species of medical importance

Bacillus anthracisBacillus cereus

Bacillus anthracis

facultativelarge, block shaped

rodscentral spores

develop under all conditions except in the living body

virulence factors capsule & exotoxins

Bacillus anthracis3 types of anthrax

Cutaneous spores enter through skin,

black soreleast dangerous

Pulmonary inhalation of spores

Gastrointestinal ingested spores

treated with penicillin or tetracycline

http://www.youtube.com/watch?v=mi3sYzDsSGI

Bacillus cereus

common airborne & dustborne

grows in foods, spores survive cooking & reheating

ingestion of toxin-containing food causes nausea,

vomiting, abdominal cramps & diarrhea

24 hour durationno treatmentspores abundant in the

environment

Clostridiumgram-positivespore-forming rodsAnaerobic 120 speciesoval or spherical spores produced only under

anaerobic conditionscause wound & tissue infections and food intoxications

C. difficileC. botulinumC. perfringensC. tetanis

Clostridium difficile-Associated Disease (CDAD)

Normal resident of colon, in low numbers

Causes antibiotic-associated colitis relatively non-invasive treatment with broad-spectrum

antibiotics kills the other bacteriaallowing C. difficile to

overgrow Produces enterotoxins that

damage intestines Major cause of diarrhea in

hospitals Increasingly more common in

community acquired diarrhea

Clostridium botulinum

Anaerobic, endospore-forming, Gram-positive bacillus

Common in soil and waterBotulism results when the endopsores germinate

and produce botulism toxins

Clostridium botulinum

Causes 3 diseases1. food poisoning

o spores are in soil, may contaminate vegetables

o improper canning does not kill spores & they germinate in the can producing botulinum toxin

toxin causes paralysis by preventing release of acetylcholine

2. infant botulism o caused by ingested spores that germinate & release

toxin

3. wound botulismo spores enter wound & cause food poisoning symptoms

Clostridium botulinumDiagnosis

Symptoms are diagnostic

TreatmentAdminister neutralizing antibodies against botulism

toxinAdminister antimicrobial drugs in infant botulism cases

PreventionProper canning of foodInfants under 1 year should not consume honey

Gangrene Mass of body tissue dies (necrosis)Usually occurs when blood flow ceases to a

part of the body

Types :Gas gangrene (myonecrosis)

caused when spores enter the body through a severe open wound

Dry gangreneWet gangrene

Clostridium perfringens

Clostridium perfringens

Vegetative cells ferment muscle carbohydrates and decompose muscle proteins

Large amounts of gas accumulate under the skin causing a crackling sound

-toxin damages and lyses blood cells

Treatment involves:Antibiotics tissue debridementAmputationexposure in a hyperbaric

oxygen chamber

Clostridium tetani

Tetanus Causes hyperactive muscle contractions

Spores can enter the body through a woundproduce toxins

• Tetanospasmin inhibits compounds needed to inhibit muscle contraction

Symptoms of tetanus include:Trismus (lockjaw)

involves spasms of the jaw muscle and clenching of the teeth

Opisthotonusinvolves muscle spasms that cause an arching of the back

Spasmodic inhalation and seizures in the diaphragm and rib cagereduces ventilation

Sedatives, muscle relaxants, and penicillin are used in treatment

Tetanus toxoid is used in vaccination

Clostridium tetani

Listeria monocytogenesnon-spore-forming gram-positive

coccobacilli 1-4 flagellano capsulesresistant to cold, heat, salt, pH extremes &

bileprimary reservoir is soil & watercan contaminate foods & grow during

refrigeration

Listeria monocytogenes

Listerosis immunocompromised patients,

fetuses & neonates affects brain & meninges

20% death rate

ampicillin & trimethoprim-sulfamethoxazole

Prevention pasteurization & cooking

Mycoplasmas

M. pneumoniae primary atypical

pneumoniaWalking pneumonia

pathogen slowly spreads over interior respiratory surfaces

causes fever, chest pain and sore throat

Corynbacterium diptheriae

gram-positive irregular bacilli 2 stages of disease:

1. Local infection –upper respiratory tract inflammation

– sore throat, nausea, vomiting, swollen lymph nodes, pseudomembrane formation can cause asphyxiation

2. Diptherotoxin production and toxemia target organs primarily heart and

nerves

Epidemiology and Pathology

Reservoir of healthy carrierspotential for diphtheria

is always presentMost cases occur in non-

immunized children living in crowded, unsanitary conditions

Acquired via respiratory droplets from carriers or actively infected individuals

Corynbacterium diptheriae

Diagnostic methods Pseudomembrane and swelling indicativeStainsConditions, historySerological assay

Treatment:AntitoxinPenicillin or erythromycin

Prevented by toxoid vaccine series and boosters

Mycobacterium Genus

gram-positive irregular bacilliacid-fast stainingstrict aerobes produce catalasepossess mycolic acids & a unique type of

peptidoglycando not form capsules, flagella or sporesgrow slowly2 medically important:

Mycobacterium tuberculosisMycobacterium leprae

Mycobacterium tuberculosis

contain complex waxes & cord factor prevent destruction by

lysosomes of macrophages

transmitted by airborne respiratory droplets

only 5% infected people develop clinical disease

Primary TB

infectious dose 10 cellsphagocytosed by

alveolar macrophages multiply intracellularly

after 3-4 weeks immune system attacks, forming tuberclesgranulomas consisting

of a central core containing bacilli surrounded by WBCs

Secondary TB

reactivation of bacillitubercles expand & drain into the

bronchial tubes & upper respiratory tractgradually patient experiences more

severe symptomsviolent coughing, greenish or bloody sputum,

fever, anorexia, weight loss, fatigueuntreated 60% mortality rate

Extrapulmonary TB

during secondary TB, bacilli disseminate to regional lymph nodes, kidneys, long bones, genital tract, brain, meninges

these complications are grave

Diagnosis

1. in vivo or tuberculin testing

2. X rays

3. direct identification of acid-fast bacilli in specimen

4. cultural isolation and biochemical testing

Treatment of TB

6-24 months of at least 2 drugs from a list of 11

one pill regimen called Rifater (isoniazid, rifampin, pyrazinamide)

vaccine based on attenuated bacilliCalmet-Guerin strain of M. bovis used in

other countries

Mycobacterium leprae

Hansen’s bacillusstrict parasite slowest growing of all speciesmultiplies within host cells in large packets

called globicauses leprosy

chronic disease that begins in the skin & mucous membranes & progresses into nerves

Leprosy (Hansen’s Disease)

spread through direct inoculation from leprotics

2 formstuberculoid

superficial infection without skin disfigurement

damages nerves and causes loss of pain perception

lepromatous deeply nodular infection causes severe disfigurement of the

face & extremities

Diagnosing

Combination of symptomology, microscopic examination of lesions, and patient history

Detection of acid-fast bacilli in skin lesions, nasal discharges, and tissue samples

Treatment and Prevention

Treatment by long-term combined therapy

Prevention requires constant surveillance of high risk populations

WHO sponsoring a trial vaccine

Gram-negative Cocci and Bacilli

Bacterial Meningitis

meninges of brain and spinal cordcross the blood-brain

barrier

can be caused by several bacterial speciesNeisseria meningitides Streptococcus

pneumoniaeHaemophilus influenzae

Neisseria

Gram-negative diplococcinone develop flagella or sporescapsules on pathogensStrict parasites

do not survive long outside of the hostResidents of mucous membranes of warm-blooded

animalsAerobic or microaerophilicPathogenic species require enriched complex media and

CO2

2 primary human pathogens Neisseria gonorrhoeae Neisseria meningitidis

Neisseria meningitidis

Virulence factors capsule, pili, IgA protease

12 strainsserotypes A, B, C, cause most cases

Disease begins when bacteria enter bloodstream, pass into cranial circulation, multiply in meningesvery rapid onsetendotoxin causes hemorrhage and shockcan be fatal

Treated with penicillin, chloramphenicolVaccines exist for group A and C

Neisseria gonorrhoeae

Causes gonorrheaVirulence factors

pili, other surface molecules, IgA proteaseStrictly a human infectionIn top 5 STDsInfectious dose 100-1,000Does not survive more than 1-2 hours on

fomitesInfection is asymptomatic in 10% of males and

50% of females

Gonorrhea

Males urethritis, yellowish

discharge, scarring & infertility

Extragenital infectionsanal, pharygeal,

conjunctivitis, septicemia, arthritis

Gonorrhea

Females vaginitis, urethritis,

salpingitis (PID) mixed anaerobic abdominal infection

common cause of sterility & ectopic tubal pregnancies

Gonorrhea in Newborns

Infected as they pass through birth canal

Eye inflammation, blindness

Prevented by prophylaxis after birth

Diagnosis and Control

Gram stain20-30% of new cases are

penicillinase-producing PPNG or tetracycline resistant TRNG

Recurrent infections can occur

Reportable infectious disease

Enterobacteriaceae Family

Enterics gram-negative bacteria many members inhabit soil,

water, & decaying matter cause diarrhea through

enterotoxins divided into coliforms (lactose

fermenters) and non-coliforms (non lactose fermenters)

Antigens and virulence factors of typical enteric bacteria

Testing of Enterics

miniaturized, multichambered tube inoculating rod pulled through length of

tubecarries an inoculum to all chambers

Coliform Organisms and Diseases: Escherichia coli

most common aerobic & non-fastidious bacterium in gut

@ 150 strainsMost not infectious

Escherichia coli

enterotoxigenic E. coli causes severe diarrhea due to heat-labile toxin &

heat-stable toxin stimulate secretion & fluid lossalso has fimbrae

enteroinvasive E. coli causes inflammatory disease of the large intestine

enteropathogenic E. coli linked to wasting from infantile diarrhea

Enterohemorrhagic E. coliNewest strainCan permanently damage kidney

Escherichia coli

pathogenic strains frequent agents of infantile diarrhea greatest cause of mortality among babies

causes ~70% of traveler’s diarrheacauses 50-80% UTIindicator of fecal contamination in water

Other Coliforms

Serratia marcescensproduces a red pigmentcauses pneumonia,

burn & wound infections, septicemia & meningitis

Klebsiella pneumoniae

Citrobacter opportunistic UTIs &

bacteremia

Salmonella

S. enteritidis 1,700 serotypes salmonellosis zoonotic gastroenteritis 2-5 days

Typhoid Fever

caused by Salmonella enterica serotype Typhi (S. typhi) typhoid fever ingested bacilli adhere to small

intestine cause invasive diarrhea that leads

to septicemia

S. Typhi is transmitted by the five Fs: Flies Food Fingers Feces Fomites

Shigella

shigellosis incapacitating dysentery

S. dysenteriae, S. sonnei, S. flexneri & S. boydii

produce H2S or ureaseNonmotilenonencapsulated

Shigella

invades villus of large intestinecan perforate intestine or invade blood

enters Peyer’s patches & instigates inflammatory response endotoxin & exotoxins

treatment fluid replacement & ciprofloxacin & sulfa-trimethoprim

Yersinia pestis

tiny, gram-negative rodunusual bipolar staining & capsulesvirulence factors

capsular & envelope proteins protect against phagocytosis & foster intracellular growth

coagulase

Yersinia pestis

sylvatic plague humans develop plague through contact with wild

animals urban plague

domestic or semidomestic animals or infected humansfound in 200 species of mammals

rodents harbor the organism but do not develop the disease

flea vectors bacteria replicates in gut, coagulase causes blood

clotting that blocks the esophagus flea becomes ravenous

Pathology of Plague bubonic

bacillus multiplies in flea bite, enters lymph, causes necrosis & swelling in groin or axillabubo

septicemic progression to massive bacterial growth virulence factors cause intravascular

coagulation subcutaneous hemorrhage & purpura black plague

pneumonic infection localized to lungs, highly

contagious fatal without treatment

Plague

Treatmentstreptomycin,

tetracycline or chloramphenicol

Killed or attenuated vaccine

http://www.youtube.com/watch?v=9IjhQDnoCcY

Bordetella pertussis

aerobic coccobacilluscauses pertussis or whooping cough

communicable childhood affliction acute respiratory syndromeoften severe, life-threatening complications in

babiesreservoir

apparently healthy carrierstransmission by direct contact or inhalation of

aerosols

Bordetella pertussis

virulence factorsreceptors that recognize & bind to ciliated

respiratory epithelial cellstoxins that destroy & dislodge ciliated cells

DTaP vaccine acellular vaccine contains toxoid & other Ags

Pseudomonas

small gram-negative bacilli single polar flagellumhighly versatile metabolism

Pseudomonas aeruginosa

intestinal resident in 10% normal peopleresistant to soaps, dyes, quaternary

ammonium disinfectants, drugs, dryingUse aerobic respiration

do not ferment carbohydrates

Opportunistic

Pseudomonas aeruginosacommon cause of nosocomial infections in hosts

with burns, neoplastic disease, cystic fibrosiscomplications include pneumonia, UTI,

abscesses, otitis, & corneal diseasegrapelike odorgreenish-blue pigment (pyocyanin)multidrug resistant

Francisella tularensiscauses tularemia

zoonotic disease of mammals (particularly rabbits)endemic to the northern hemisphere

Aerobic bacillitransmitted by contact with infected animals,

water & dust or bites by vectorsheadache, backache, fever, chills, malaise &

weaknessintracellular persistence can lead to relapse30% death rate in systemic & pulmonic forms

gentamicin or tetracycline

Mycoplasma pneumoniae Legionella pneumophilaCoxiella burnetiiChlamydia pneumoniaeChlamydia psittaci

“Atypical” Pneumonia Can Be Caused by a Diverse Group of Bacterial Species

Legionella pneumophila

“Legionellosis”, Legionaires disease

Motile aerobic bacilliwidely distributed in water live in close association with

amebasprevalent in males over 50nosocomial disease in elderly

patients fever, cough, diarrhea,

abdominal pain, pneumonia fatality rate of 3-30%azithromycin

Rickettsias, Chlamydias, Spirochetes and Vibrios

Rickettsia

obligate intracellular parasitesgram-negative cell wallamong the smallest bacterianonmotile pleomorphic rods or coccobacilliticks, fleas & louse are involved in their life cycle bacteria enter endothelial cells & cause necrosis

of the vascular lining treat with tetracycline & chloramphenicol

4 Types of Rickettsioses

Rocky Mountain spotted fever R. rickettsii zoonosis carried by dog ticks & wood ticks most cases on eastern seaboard distinct spotted rash

Chlamydias

obligate intracellular parasites

small gram-negative cell wall

alternate between 2 stageselementary body

small metabolically inactive, extracellular, infectious form

reticulate body grows within host cell

vacuoles

Chlamydia trachomatis 1. trachoma

attacks the mucous membranes of the eyes, genitourinary tract & lungsocular trachoma

• severe infection, deforms eyelid & cornea, may cause blindness

inclusion conjunctivitis • occurs as babies pass through birth

canal• prevented by prophylaxis

2. STD urethritis, cervicitis, scarring lymphogranuloma venereum

disfiguring disease of the external genitalia & pelvic lymphatics

Spreading to the fallopian tubes can cause salpingitis

Left untreated can cause pelvic inflammatory disease (PID)

Increases the danger of infertility or ectopic pregnancies

Chlamydia can also occur in the pharynx or anus

Males complain of painful urination and watery dischargecause infertility in males

Spirochettes

Treponema

Borrelia

Treponema

Gram-negative spirochetes live in the oral cavity, intestinal tract, &

perigenital regions of humans & animalspathogens are strict parasites

Treponema pallidum

human is the natural hostextremely fastidious &

sensitivecannot survive long outside

of the hostcauses syphilis ID = 50 cells

Pathogenesis and Host Response

Spirochete binds to epithelium, multiplies, and penetrates capillaries.

Moves into circulation and multiplies Untreated marked by stages

PrimarySecondaryTertiary

Spirochete appears in lesions and blood during first 2 stages communicable

Stages of Syphilis

Primary syphilis appearance of hard

chancre at site of inoculation

chancre heals spontaneously

Secondary syphilis fever, headache, sore

throat, red or brown rash on skin, palms and soles

rash disappears spontaneously

Stages of Syphilis

Tertiary syphilis about 30% of infections enter

in tertiary stage can last for 20 years or longerneural, cardiovascular

symptoms, gummas developCongenital syphilis

nasal discharge, skin eruptions, bone deformation, nervous system abnormalities

Borrelia

Borrelioses Gram-negative spirochetestransmitted by arthropod vectorB. hermsii

relapsing fever

B. burgdorferi Lyme disease

B. hermsii - Relapsing Fevermammalian reservoirs

squirrels, chipmunks, wild rodentstick-borneafter 2-15-day incubation, patients have high

fever, shaking, chills, headache, & fatigueNausea, vomiting, muscle aches, abdominal

painextensive damage to liver, spleen, heart, kidneys, &

cranial nervesparasite changes & immune system tries to

control itrecurrent relapses

tetracycline

B. burgdorferi - Lyme Disease

transmitted by tickscomplex 2-year cycle

involving mice & deernonfatal, slowly

progressive syndrome that mimics neuromuscular & rheumatoid conditions

B. burgdorferi - Lyme Disease

Symptoms:70% get bull’s eye rash fever, headache, stiff

neck, & dizziness if untreated can progress to

cardiac & neurological symptoms, polyarthritis

tetracycline, amoxicillinvaccine for dogs, human

vaccine discontinued insect repellant containing

DEET

Vibrio cholera

CholeraCurviform gram-

negativetop 7 causes of

morbidity & mortalityingested with food or

waterinfectious dose 108

Vibrio cholera

infects surface of small intestine, noninvasive

cholera toxin causes electrolyte & water loss through: secretory diarrhea, resulting dehydration leads

to muscle, circulatory, & neurological symptomsTreatment

oral rehydration, tetracyclinevaccine

Campylobacter jejuni

important cause of bacterial gastroenteritis

transmitted by beverages & food

Curviform gram-negative reach mucosa at the last

segment of small intestine near colonadhere, burrow through

mucus and multiplysymptoms of headache,

fever, abdominal pain, bloody or watery diarrhea

Helicobacter pylori

Curviform gram-negativediscovered in 1979 in stomach biopsied

specimens causes 90% of stomach & duodenal ulcerspeople with type O blood have a 1.5-2X

higher rate of ulcersSame receptor in common

produces large amounts of urease

The bacteria produce urease, which in turn produces ammonianeutralizes acid in

that area of the stomach

allows the bacteria to survive

The ammonia, and an H. pylori cytotoxin destroy mucous-secreting cellscreates a sore

© P. Hawtin/Photo Researchers, Inc.