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43 Cards in this Set

  • Front
  • Back
Bacillus anthracis (G+)
Spore forming, G+ rod, aerobic
Common in livestock (cattle, horses, sheep)
First bacteria proven to cause disease
2001 bioterrorism attack
Not spread human-human

Disease from contact with infected herbivores or indirectly via their products

1. Cutaneous anthrax
Handling infected material
95% cases
2-3 day incubation
Initial skin papule (small, hard raised area developing into thick, dry, black necrotic tissue (in few days)
20% untreated cases progress to fatal septicemia (meningitis)

2. Intestinal anthrax
Eating infected meat
Same as cutaneous, but on intestinal mucosa
60% fatal (untreated)

3. Pulmonary anthrax
Inhaling spore-laden dust
Spores – macrophage – lymph system – germination - systemic
Nearly 100% fatal (untreated)

For both intestinal and pulmonary, symptoms usually mild at first (low fever, malaise, GI problems). Followed by sudden onset of high fever, disorientation, cyanosis (blue discoloration of skin due to loss of oxygen), shortness of breath and coma/death within few hours

Virulence
Capsule (prevents phagocytosis)
Toxin: organ destruction esp spleen

Penicillin very effective
B. Cereus (G+)
B. cereus – known mainly for food poisoning (2-5%)
Diarrheal 8-16 hours after consumption (spore germinating in body)
Or
Nausea and vomiting 1-5 hours after consumption (toxin in food)

Common in rice (cooked – stored at room temp – spore germinates and releases toxin – ingested toxin)

May be associated with abscesses, wound infections, burn infections, ear infections, endocarditis, meningitis – all esp in immunocompromised
Variety of foods
C. Botulinum (G+)
G+ rod anaerobic, spore forming

Food poisoning (canned foods, sensitive to high acid or high sugar, heating)
Preformed toxin
Incubation typically 18-36 hours
Early GI problems (nausea, vomiting, abdominal pain) – toxin enters blood – attacks peripheral nerves – Flaccid musle paralysis (blocks acetylcholine release) – blurred vision, dilated pupils, slurred speech, dry mouth, overall weakness – death due to respiratory failure
Treat with stomach lavage and enemas, antitoxin
15% fatal
Wound botulism (rare)
Contamination of wound
incubation days-weeks
No GI distress
Infant botulism (2-6 month old)
Germination of spores in GI tract (undeveloped)
Raw honey is the most frequent cause
Constipation – lethargic – drooling – loss of head control, flaccid, respiratory arrest
4-15% cases of sudden infant death
Antibiotics/antitoxin

Medical use
Migraine headaches
Involuntary contraction of eye muscles
Excessive sweating
Neuromuscular disorders
Cosmetic

Lasts about 6 weeks
C. Tetani (G+)
Common soil organism
Enters through wound, secretes toxin causes muscle spasms
Cramping and twitching of muscles around wound – sweating – pain around wound and neck/jaw(Lockjaw) – portions of body become rigid (muscle contraction) –pulmonary/cardiac failure
40-90% fatal if untreated
1 million cases/yr world (a leading cause of death in developing countries)
Vaccine available (treatment as well), penicillin
Boost every 10 years
C. Dificile (G+)
Normal flora in 3% adults
Severe infection of colon (often after antibiotic therapy)
Nosocomial
13% patients in two weeks
50% patients in 4 weeks
Symptoms vary (mild diarrhea to severe abdominal pain with fever and weakness due to toxin)
5-10% patients have bloody diarrhea
Distinctive foul stool odor
May have pseudomembranous colitis (white/gray patches on colon mucosa filled with leukocytes and mucus)
Can be lethal
Detection by bacterium/toxin in stool (ELISA)
Symptoms often resolve after use of antibiotic (1-14 days)
Can use vancomycin to treat
Supplements of lactobacillus
C. Perfringens (G+)
Clostridium perfringens
Food poisoning
Third most common food borne illness (usually meat)
Toxin reasonably heat resistant
Incubation 8-16 hours, lasts 24 hours
Abdominal pain, diarrhea (not lethal)
Most people have antibody to toxin (exposed during life)

Gas gangrene
1000 cases/yr US
Often fatal
Wound – impairs blood supply (lack of oxygen) – bacterial growth – fever and pain at site – spread and necrosis of tissue – muscle discoloration (purple mottling) and foul smelling due to anaerobic fermentation (gas bubbles form)

Incubation 1-6 days
May cause death within hours after incubation period
Penicillin and often removal of infected tissues
L. Monocytogenes (G+)
G+ rod
Listeriosis
2500 cases/yr US
Eating contaminated food
Soft cheeses, pates, raw milk, uncooked or meat stored for long time in fridge
Primarily a problem in pregnant women, newborns and immunocompromised
Usually asymptomatic in all others
Mild flu initially (fever, muscle aches) – Meningitis (stiff neck, headache, confusion, loss of balance)
(Pregnant women – mild symptoms, but to fetus – abortion, stillbirth)

Present in raw contaminated food
Can grow at low temps (in refrigerator)

Virulence factors:
Secretes toxin (invasion) to penetrate epithelial lining
- can replicate intracellularly in macrophages after phagocytosis
Toxin (listerolysin) – escape phagolysosome inside macrophage
Produce catalase (to block phagocytic digestive activity)

Produce Act A (form actin inside infected cell pushing bacteria into a new cell)

Ampicillin, vanocomycin

FDA approved bacteriophage treatment
Corynebacterium diphtheriae (G+)
Corynebacterium diphtheriae
G+ rod, grouped into “Chinese letter” shapes
Toxin released
Infects nasopharynx – sore throat, malaise, fever, swelling of neck (Bull neck) – difficult breathing/swallowing
Thick gray membrane (pseudomembrane) often forms in upper resp tract – can obstruct breathing
Spread by droplets, secretions and direct contact (highly contagious)
Can become severe/life threatening – loss of motor function and congestive heart failure
Human-human only
Vaccine available
To toxin (not bacteria), 97% effective
Prevaccine: 200,000cases/yr, 15,000 deaths US
5 cases since 2000
Treatment
Vaccine or penicillin
Staphylococcus Aureus (G+)
G+ cocci, grape-like clusters
Catalase positive (Strep – catalase negative)
Coagulase positive (most other Staph is negative)
Growth on high salt
Beta hemolysis
Entry: wounds or nasal/mucosal
25% pop carrriers

*Superficial skin lesions and deep infections
*Common cause of food poisoning (abrupt/violet onset
Severe nausea, vomiting, diarrhea 1-2 days)
*Pneumonia, deep abscesses, endocarditis, meningitis, osteomyelitis (infection of bone marrow)
Often associated with indwelling devices (joint prosthesis, heart valves)

Virulence factors
Proteins for attachment
Factors to block phagocytosis
Capsule
Protein A - to bind IgG
Toxins
Alpha toxin – septic shock
Decreased oxygen delivery, vasodilation
Leukocidin
Destroy leukocytes
Toxic shock syndrome toxin (TSST)
Superantigen (stimulate dramatic T-cell response)
1980s – some tampons allowed rapid growth of S. aureus
Enterotoxin
Diarrhea and vomiting (food poisoning)

Common nosocomial and environmental
Many antibiotic resistant
MRSA – methicillin resistant and multiple resistance
80,000 nosocomial infections/yr

20,000 deaths, ½ nosocomial
- worse than AIDS = 17,000 deaths/ yr US

Treatment: vancomycin
Staphylococcus epidermidis (G+)
Usually apathogenic
Can form biofilm (catheter problems and indwelling devices)
Staphylococcus saprophyticus (G+)
UTIs
Esp in females 17-27 years old
Burning urinations, urge to urinate often
Streptococcus Pyogenes (G+)
G+ chains
Catalase negative (all streps)
5-15% humans have as normal flora
Pharyngitis (strep throat) or Tonsillitis
Sore and red throat, pain on swallowing, high fever, headache, nausea, vomiting, malaise
Impetigo (skin infections)
Pimple-like lesions surrounded by reddened skin. Lesions fill with pus, then break down over 4–6 days and form a thick, honey-colored crust.
Scarlet fever
“strep throat” with rash on upper body, White coating on the surface of the tongue. The tongue itself looks like a strawberry because the normal bumps on the tongue look bigger
Pyrogenic exotoxin – causes rash

Invasive diseases (10,000 cases/year US, 1,000 deaths)
Necrotizing fasciitis
Deep infection of subcutaneous tissue
Extensive destruction of muscle and fat tissue
Multi-organ failure (50% fatal)
Superantigen – tissue damage
Severe pain and swelling, often rapidly increasing, fever, redness at wound site
25% fatal
Streptococcal toxic shock syndrome (STSS)
rapid drop in blood pressure and organs
Fever, dizziness, Abrupt onset of severe pain, often in an arm or leg, confusion, A flat red rash over large areas of the body
35% fatal
Other:
Rheumatic fever (autoimmune disease)
Chronic disease of heart and valves
No bacteria in heart, but follows repeated attacks of strep throat
Apparently similar bacterial antigen to self

Virulence
Capsule
M-protein (attachment to mucous membrane, block complement)
Toxins
Streptolysins (kill leukocytes)
Hyaluronidase (Digest connective tissue)
Streptokinase (decrease clotting)
Superantigens
Usually treated with penicillin or clindamycin
Streptococcus Pneumoniae (G+)
20-40% humans have as normal flora

Most common cause of community acquired pneumonia
(0.5 million/yr US)
Pneumonia progresses vary rapidly with a sudden onset of high fever. Infection can become invasive (bloody sputum/cough)- meningitis
Most common cause of sinusitis and conjunctivitis (after childhood) - 7 million/yr US

Increasing cause of meningitis (3000/yr US)

Capsule important
Toxin: Autolysin – lysis of own cells which are no longer dividing (stationary phase) – role to release bacterial components and cause increased human cell death (immune response and more bacterial toxins)

100,000 cases/year US pneumonia (3300 meningitis)
Penicillin resistant
Vaccine available (since 2000)
Esp for meningitis
Streptococcus Mutans (G+)
Streptococcus mutans (viridins group)
Problem in dental work
Dental plaque and caries (due to lactic acid production)
Can lead to transient bacterimia and heart disease
Enterococcus faecalis (group D) (G+)
98% of enterococcal infections – Diverticulitis (inflammation of Lg intestine, Abdominal pain, constipation, nausea)

Normal GI flora
Nosocomial infections - VRE (vancomycin resistance enterococcus)
Major cause of endocarditis
Also urinary tract, wound infections (high fever, sweating, dilated pupils), meningitis
Streptococcus agalactiae (group B) G+
Neonatal disease (usually during birth)
Pneumonia or meningitis
fever, vomiting, poor feeding, and irritability
High mortality
Penicillin (tetracycline resistant)
Bordetella pertussis G-
Whooping cough
Acute respiratory, severe coughing episode
Complications: bronchial pneumonia, acute encephalopathy (rare)
Killed 5000-10000/yr US before vaccine (now less than 100)
G- coccobacilli

Virulence
Pertussis toxin
Attachment to human cilia (block cilia movement)
Leads to increase in mucous secretions
Adenylate cyclase toxin
Inhibits phagocytic cell digestion (oxidative response)
Filamentous hemagglutinin
Attachment to human cilia
Hemolysin
Lyse RBC – obtain iron and nutrients
Symptoms
Initially runny nose, sneezing, mild cough, and low-grade fever
- severe coughing, pneumonia
-characteristic ‘whoop’ sound when inhaling

Transmission by droplets (person-person)
Can only colonize ciliated epithelial cells of respiratory mucosa
Bacteremia does not occur
Most infectious during early phase but remain infectious for 5 weeks (entire infection)
Common childhood disease before vaccine
Incubation 1-2 weeks
Vaccine
Diptheria, tetanus, pertussis (killed vaccine) – 85% US vaccinated (20% mild side effects, 0.1% convulsions)
Treatment: erythromycin
2010: 10,000 cases in CA, 2012: 1,500 cases in WA
Chlamydia Trachomatis G-
G-indeterminate cocci (hard to stain, structure G-)
C. trachomatis –
- conjunctivitis
Most common preventable cause of blindness in world (15% cases, just below cataracts)
Spread by touching eye or birth canal
- Genital infection
Common STD (4 million cases/yr US) – most frequenty reported STD
½ men, ¾ women asymptomatic “Silent epidemic”

-Women: pelvic inflammatory disease (infection of uterus, fallopian tubes or ovaries) - infertility
Urethritis: Vaginal discharge (milky white/yellow), painful urination

-Men: epididymitis (inflammation of coiled tube on back of testis); urethritis (swelling of the urethra) – penis discharge (typically white), painful urination
5X more likely to become infected with HIV

Obligate INTRACELLULAR
Cannot replicate on own (needs ATP from cell)
Infects epithelial cells
1-3 week incubation period

Virulence factor
Hemagglutinin – attachment to cells
Tissue damage due to cell mediated immune response

Worldwide (prevalence in Africa and Asia)

Antigen test available for detection
Treatment
Tetracycline (penicillin resistant)

C. pneumoniae – atypical pneumonia
By inhalation
Typically mild
E. Coli G-
G- rod
Common normal flora
Virulent strains possess novel genetic elements (ie, plasmids)
- noninflammatory diarrhea (watery)
- inflammatory diarrhea (with blood, mucous, leukocytes)

Transmission fecal-oral
Pili allows colonization of ilium

Infection common in poor sanitation, traveling to developing
countries (“travelers diarrhea)
Meat, milk. Water. veg
Disease most serious in infants

GROUPS:
Enterotoxigenic (ETEC)
Watery diarrhea, nausea, no-low fever
Travelers diarrhea
Toxin to damage mucosal cells, secretion of water and electrolytes (LT and ST toxins – shiga-like)
Lasts 24-72 hours
Non invasive (do not enter cells)

Enteroinvasive (EIEC)
Dysentary (with blood and mucous), fever
Secrete invasive factors
Identical symptoms to shigellosis
Invade host cells (have adhesion protein)

Enteropathogenic (EPEC)
Profuse watery diarrhea, fever (occasional bloody)
Common in newborn nurseries and nosocomial
Unknown toxin
Moderately invasive

Enterohemorrhagic (EHEC)
O157:H7 – serologic group
Bloody diarrhea, NO fever, abdominal pain
Mainly food borne
Shiga-like toxin (A-B subunits)
Can cause kidney failure
Toxin causes intense immune response
Moderately invasive
73,000 cases/yr; 61 deaths/yr
2011: Germany 3,800 cases, 45 deaths (from bean sprouts)

Uropathogenic E. coli (UPEC)
Causes 90% of urinary tract infections in normal individuals
Colonize in urethra and into bladder
Women 14X more likely due to shorter urethra and proximity of anus to urethra

Treatment: amoxicillin
Phage – approved Jan 2007 (US) to be used on meat for human consumption
Called Vero toxin
Salmonella Enteritidis G-
Gram – rod

Non-typhoid
Gastroenteritis (diarrhea, abdominal cramps, fever)
Worldwide
Animals are main reservoir (turtles, fowl)
Food borne usually (rare person-person)
2 million cases/yr US
Salmonellosis
6-48 hour incubation after food intake
Nausea, vomiting diarrhea, abdominal pain, headache, fever
Lasts 2-7 days

Food:
41% turkeys positive
50% chickens
21% eggs
Jalapenos, peanut butter, cantelopes
Salmonella typhi G-
Salmonella typhi G- Rod
Typhoid fever (Enteric fever)
Person-person (via fecal oral contamination)
No significant animal reservoir
Carriers can be asymptomatic (“Typhoid mary”) 3% people asymptomatic may last weeks-months
Incubation 10-14 days (may be preceded by gasteroenteritis) Sudden fever, anorexia, headache, myalgia (muscle pain), constipation
Can be fatal
Vaccine available (partially effective)
25 million cases/yr worldwide (500,000 deaths)
1% fatal if treated, 25% fatal if untreated
Ciprofloxacin
Cystic fibrosis patients immune (need CFTR for entry)
Virulence due primarily to adherance

Pathogenesis dependent on
1. ability to invade and replicate inside cells
2. LPS layer

***After ingestion, colonize ileum – invade epithelium cells – reticuloendothelial space – can infect deeper tissues of the spleen, liver, and the bone marrow
Shigella dysenteriae G-
Shigellosis – abdominal pain, bloody, mucoid diarrhea
Abdominal tenderness, fever, vomiting, dehydration

G- rod
Fecal – oral
Endemic in poor sanitation areas
50% of bloody diarrhea in small children due to Shigella
448,000 cases/yr

Ampicillin, trimethoprim, ciprofloxacin

Incubation 24-48 hours
Mild – watery diarrhea
Severe – dysentery
Lasts 7 days

Very similar to enteroinvasive E. coli (EIEC)

Invades colon epithelium (unique- most bacteria in small intestine/ileum)– and invade subepithelial space
If phagocytosed by macrophage – block degradation
All lead to massive inflammation and cell death

Toxin – leads to fluid accumulation
Shiga-toxin (A-B toxin: A=active portion, B=binding portion)
Yersinia Pestis G-
G- Bubonic plague
Transmitted by bite of infected rat flea (rat pathogen)
Swollen blackened lymph nodes develop (Buboes)
- septicemia and hemorrhagic pneumonia and death
- Visible skin darkening
Up to 90% mortality if untreated (pneumonia)
Pneumonic plague
Person-person (droplets)
Occurs during epidemic
100% mortality
Can die within 24 hours after symptoms
Diagnose via bacteria in sputum


Gram – coccobacilli
Responsible for death of 1/3 population during Middle Ages (1300s)
(25 million deaths)

Produces two antiphagocytic proteins
Only at 37oC
F1 – blocks phagocytosis
V&W – blocks lysosome

Streptomycin, gentamycin (only few antibiotic resistance)
Yersinia enterocolitica G-
G-
Y. enterocolitica
Relatively uncommon, Severe diarrhea with abdominal pain
Raw or undercooked pork products
Deer/cattle pathogen (contaminated water)
Haemophilus Influenza G-
Acute bacteria meningitis
Until vaccine, most common cause of meningitis in children

G- coccobacilli
Normal flora: 75% pop carriers

Colonize nasopharynx – penetrate epithelium – bacteremia - meningitis
Headache, stiff neck, epiglottitis (swelling of epiglottis (throat) to the point of choking)
Infections of the blood, joints, bones, and covering of the heart
Pneumonia (thought originally to be cause of flu infections)

Spread via direct contact, secretions, aerosol

Diagnosis via bacteria in blood or cerebrospinal fluid (growth, antigen test of PCR)

*Requires hemin (factor X) and NAD+ (factor V) for growth
NAD+ from blood cells
Hemin from lysed blood cells
(use Chocolate agar for growth – lysed RBCs in media)

*Capsule needed for virulence
No known exotoxins
IgA protease

Ampicillin or cephalosporin (increasing resistance to Amp)
Treated: 10% fatal

Vaccine: polysaccharide only (Hib vaccine – type b)
Prevaccine: 20,000 cases/yr US
Postvaccine: 100 cases/yr
Heliobacter pylori G-
Associated with stomach inflammation
Peptic ulcer disease
Gastric carcinoma
Acute infection: vomiting, upper GI pain

G- curved rod, flagella to penetrate mucous lining

Sheltered from gastric acidity
Only known organism known to thrive in stomach environ.
“drills” into mucous layer of gut and attaches to cells
Does not invade tissue
Produces urease (which degrades urea from stomach producing
Ammonia and CO2) - ammonia toxic to cells and
leads to epithelium damage
Ammonia also buffers acidity to help bacteria survive

Possibly infectious (poor sanitation areas – 90% infected)
Fecal-oral

Normally 30% pop infected (70% assymtomatic)


Serological tests are now available (antibodies in serum)

Treatment:
omeprazole (proton pump inhibitor) + amoxicillin, and clarithromycin for 10 days;
bismuth subsalicylate (neutralize acid) + metronidazole, and tetracycline (BMT) for 14 days
Campylobacter Jejuni G-
Campylobacter jejuni
G- spiral rod

Most common cause of human diarrhea
(3-14% of all cases, worldwide 4 million/yr)
Esp. in children under 2 years
Fever, malaise, abdominal pain
Can lead to relapsing ulcerative colitis (sores in colon, usually more short term)
Incubation 2-4 days
Replication in intestines

***Common in animal feces (esp birds)

Self limiting (1 week)
Relapsing: 10-20% cases

Present in water, milk, poultry, meat (contaminated from animal feces)
Treatment: erythromycin or ciprofloxacin

Link to Guillain-Barre’ Syndrome
Autoimmune toward peripheral nerves (ascending paralysis)
Related to infection (possible mycoplasma, cytomegalovirus, Epstein-Barr virus, Varicella-Zoster virus, 1976 swine flu vaccine)
Molecular mimicry
Legionella Pneumophilia G-
Acute pneumonia
Rarely endocarditis
Rarely flu-like illness called Pontiac fever
Mild illness, self limiting (fever, muscle aches, sore throat,
Cough, runny nose – upper resp, no pneumonia)

G- rod

Reside in drinking water and moist surfaces – “aerosol transmission”
(via A/C system, cooling towers) – can invade amoeba as reservoir which protects from environment/chlorination

Legionairres disease
1976 outbreak at American Legion conference in Philadelphia
221 treated, 34 deaths
A/C system
No person-person

High fever, chills, dry cough, headache, confusion – nausea, vomiting, pneumonia

After infection, engulfed by alveolar macrophage – but is intracellular parasite and multiplies inside macrophage (blocks phagocytic digestion)
- release – infect other cells
***NOT obligate intracellular parasite

Often nosocomial
10,000 cases / yr US

Detect by antiserum to microbe
Erythromycin
Mycobacterium Tuberculosis G-
Obligate aerobe
Acid fast (waxy layer)
Divides 20 hours – several days
Can survive for weeks in dry environment
G- curved rod
1/3 pop has been exposed
14.6 million active cases worldwide (rate currently dropping due to increased testing)

Chronic productive BLOODY cough, low fever, night sweats, weight loss,
fatigue

Isolates may take 4-6 weeks to grow

Airborne transmission – enter alveoli – engulfed by alveolar macrophage – replicate inside macrophage - form primary lesion – spread via lymph – reinfect lungs

Accumulation of bacteria form inflammatory focus forming \granulomatous lesion (called tubercle). Can even become calcified

5-10% develop active disease (most asymptomatic, 90%)
Persistant infection may reactivate due to immune deterioration
Diagnosis via skin test and clinical manifiestations and chest radiograph

Treatment: 6-9 months of rifampin (block dna dep RNA pol) and isoniazid
(block cell wall)
MDR-TB (resistant to these – 2% of isolates of TB)

Elderly, malnourished, alcoholics, and poor (300x greater in homeless)
In immunosuppressed – can infect CNS – meningitis and systemic
Mycobacterium Leprae G-
M. leprae
Leprosy (infection of skin, peripheral nerves and mucous membranes)
Leading to lesion, hypopigmentation, loss of sensation
Permanent damage to skin, nerves, limbs and eyes
Inflammation leads to nerve damage – numbness, paralysis, lesions, deformity

Also called Hansens disease

Transmission requires prolonged contact of individual infected

10 million cases worldwide (Asia and Africa)
Mycoplasma Pneumoniae G-
Mycoplasma pneumoniae
Smallest known bacterium

No cell wall (Gram indeterminate)

Lacks ability to make nucleotides
Obligate parasite

Invades upper and lower resp tract
Cough, fever, headache for weeks
Convalescence is slow
15-50% of all pneumonias (“walking pneumonia)

Mycoplasma sp. : Linked with several chronic diseases, including chronic fatigue syndrome, fibromyalgia syndrome, gulf war syndrome, and rheumatoid arthritis (36-50% of all patients carry Mycoplasma)
Unknown if primary cause or secondary infection

Person-person
May have asymptomatic reservoirs
Droplet spread

Incubation 2-3 weeks

Binds to and infects epithelial cells
(membrane fusion?)

Tetracycline and macrolides (no cell wall antibiotics)
Neisseria Gonorrhoeae G-
Neisseria gonorrhoeae
G- cocci, “The Clap”
Human only known host

Sexual contact
Bind epithelial cells – penetrate cells– multiply on the basement membrane
Needs pili for attachment
30-60% asymptomatic

Urethra fluid discharge (often green or yellow), difficulty urinating most common symptoms
If untreated, can become bacteremia fever, chills, hand/feet arthritis, skin lesions, pelvic pain
Incubation 2-5 days

Transmission frequency: 35-60% per sexual time
700,000 cases/yr US

Cephalosporin, doxycycline
N. meningitidis G-
Skin lesions (purple) and Acute bacterial meningitis
Lesions key to diagnosis
Distributed over body

Neck stiffness, headache, fever, purple rash (progress rapidly)
*Typically in young adults (not children)

Spread by inhalation
- attach to nasopharyngeal mucosa – cross mucosal barrier – bloodstream – CNS
Present in normal flora (5-30% people)

10% fatal with treatment
Vaccine available (meningococcal) – strains A/C (50% cases)
Penicillin

• Neisseria is difficult to grow:
• Chocolate agar (lysed RBC in media) and CO2 environment.
• Thayer-Martin agar: Chocolate agar with vancomycin to kill Gram + and Polymyxin E to kill most other Gram -
Moraxella catarrhalis (previously Neisseria catarrhalis) G-
Gram – diplococcus
Common infections of middle ear (otitis media) and sinusitis. 3-4 million cases per year in US. 70% of children will get infected

Elderly, smokers and chronic obstructive pulmonary disease (COPD) : Lower respiratory and pneumonia
(Up to 45% mortality)
Immunocompromized: pneumonia, endocarditis, septicemia, and meningitis

Emerging human pathogen (increase dramatically over past 20 years)
Normal flora in most people

Resistant to many B-lactams.
Quinolones and tetracycline useful.
Rickettsia rickettsii:
G- rod
Obligate intracellular parasite
Bite of ticks, mites (zoonotic)

Rocky mountain spotted fever
Severe human disease – 25% mortality unless treated, 4% treated
Mainly eastern US (Maryland to Georgia, Oklahoma, Missouri, Ohio, Tenn, Ark, Tex)


Bite – bloodstream – endothelium of blood vessels and smooth muscle – invade cells – damage

Damage to blood vessels leads to typical rash
Fever, rash (on extremities first), headache, nausea, muscle aches. cutaneous necrosis at bite site

Difficult to diagnose since cannot culture (need cell)
Tetracycline, chloramphenicol
R. typhi
Endemic typhus
Feces in lice and fleas – scratch –rub into wound
Headache, high fever, cough, muscle pain, chills,
Chest rash spreading to extremities
Treponema pallidum G-
syphilis
genital tract lesion – developing into disseminated lesions
1/3 people: cardiovascular and neurological problems
Pregnancy: birth defects or death

G- helical/spirochete

Lack LPS
Also very few outer proteins (not very antigenic)

Humans only reservoir

Primary stage
Incubation of 10-90 days
Skin lesion on genitalia
Enlarged lymph nodes
Last 2-6 weeks
Secondary stage
1-6 month post infection
(asymptomatic in between)
Mild fever, malaise, rash on trunk and extremities,
Mucous patches on genitals and mouth
Most infectious stage
This stage can reoccur many times
Tertiary stage
1-10+ year post infection
Any tissue may be affected
80% fatalities due to cardiovascular
Neurological (meningitis)
Joint disease

10 bacteria can cause disease


Penicillin (not yet resistant)
For 10-14 days, IV
Borrelia burgdorferi G-
Via deer tick and black-legged tick
In certain areas, 20-60% ticks carriers
Rodents are major reservoir (white footed mouse)
Deer important for tick life cycle (not carriers of Borrelia)
Lyme disease
Expanding ring-shaped red rash (in 70% patients)

G- spirochete

Bite – bloodstream - systemic

Incubation period 1 week
Generalized infection – relapsing fever, headache, muscle pain (days, weeks, months or years)
*May also have arthritis and carditis (inflammation of heart)
*Persistent neurological and arthritic infections may last years
(muscle pain, malaise - relapsing) – meningitis, mild encephalitis (leading to memory loss), Bell’s Palsy (loss of muscle tone in face)
*Possible link to lymphoma (lymphatic cell cancer)

- CHANGES antigen (allows relapsing)

30,000 cases/yr US (one of fastest growing diseases)
17,000 cases/yr in 2000
10,000 cases/yr in 1990

Often hard to diagnose (level of spirochete in blood very low), serological test typical

Early: tetracycline or penicillin
Late: ceftrixone (B-lactam) - (2 g/day, 4 weeks)
Pseudomonas aeruginosa G-
Opportunistic
Nosocomial (burns, cancer, cystic fibrosis, post-operative infection in radial keratotomy surgery patients)
50% fatality
Common in cystic fibrosis patients
Infections: endocarditis, pneumonia, UTI, wounds
“Blue-pus” in infections and sputum
G- rod

Many toxins
Protease (tissue destruction)
Hemolysin (kill macrophage)
Leukocidin (block host defense)
Pigments (anti-bacterial)
Toxin A (block host defenses)

Resistant to many antibiotics
Gentamycin, carbenicillin
Klebsiella pneumoniae G-
G- rod, ubiquitous, normal flora
Large capsule
Common cause of pneumonia
up to 50% mortality
Esp. nosocomial, link to ALCOHOLISM, diabetes (weakened immune). Gangrene in diabetics.
Common in alcoholics, immune compromised
“Currant jelly” like sputum (bloody color and thick)

Can cause urinary
tract infection
Vibrio cholerae G-
G- curved rod
Diarrhea (numorous, voluminous watery stools)
And vomiting

Incubation 6-48 hours
Initial stool: excess of 1Liter
Followed by several liters within hours

Lasts 2-7 days

Massive fluid and electrolyte loss
50% fatal without treatment

Infects only the small intestine

Toxin
Increases cAMP levels – massive fluid and electrolyte efflux

Human only host
Fecal oral contamination

Most recent epidemic in 1992 (India and Bangladesh)

Treatment
Replace fluids and electrolytes
Tetracycline
Pasteurella pneumotropica G-
Gram – coccobacilli
Opportunistic (found in commercial and research rodents)

mice, hamsters, rabbits, cats, guinea pigs, dogs
normal flora – oral, respiratory, genital, GI

Often spread via bite of animal to human

Respiratory infection (Nasal discharge, congestion, conjunctivitis)
and abscesses (can be chronic requiring surgery)
Brucella melitensis G-
Gram – coccobacillus
Zoonotic (various mammals – marine, horses, etc)
No obvious virulence factors, lives within macrophage
In US, 100-200 cases/year
Spread via infected meat and unpasteurized milk products
- typical infected food or inhalation via occupational exposure
- no human to human
Influenza-like with fever reaching 38 to 40oC.
Limb and back pains severe, sweating and fatigue
Chronic: chronic fatigue syndrome, depression, and arthritis
Can rarely lead to systemic infection in CNS (5% cases)
chronic headaches, nausea, vomiting, visual deterioration
Abortions/infertility in livestock