Enterobacteriacea Family

Orange – not bolded on slides Regular writing – bolded on slides (looked silly with most of the chart bolded) Other colours – bolded stuff with colour to make it look nicer Bacteria Properties Virulence Factors Gram (-) bacillus -Adhesions (needs to stick Escherichia Coli Outer envelope as lots of motion in Opportunistic Citochrome oxidase (-) GTU/GIT) 0157:H7 Catalase (+) -H and K antigens (variation – doesn’t stay the same) Exotoxins

Syndromes Endogenous (opportunistic): Poor hygiene/immune Pneumonia, UTIs E. Coli = 80% of community acquired Very common infection – 10-20% of women will have =>1 in life Ascending infection = anus → vagina → ureters → kidneys Special adhesions are used to attach to uroepithelium (attach to mannose) – resist flushing Sx Pyelonephritis – severe dysuria, urgency, increased frequency, incomplete voiding, fever, loin pain, (+) KI punch Septicaemia most commonly caused by E. coli (45%) Exogenous (external pathogen): Contaminated food or water Gastroenteritis – see separate chart Neonatal meningitis E.Coli and Group B Strep are most common causes E. Coli have K1 capsular Ags – get anti K1 Abs from mother through breast feeding. 5070% babies are exposed but don’t get b/c of mother’s Abs

Other ABC therapy is not indicated

Gastroenteritis M/C E. Coli infection in healthy people


ETEC/VTEC – Enterotoxigenic Traveller’s diarrhea Infant diarrhea Exotoxins ST a/ST b: heat stable, stimulate guanylyl cyclase LT I/ LT II: heat labile, stimulate adenylyl cyclase (like Cholera toxin) Watery diarrhea (*vs bloody*) Rare Vomiting

EIEC – Enteroinvasive Scant, bloody stool that is leukocyte (+) Fever Progress to colonic ulceration Similar to Shigella

EPEC – Enteropathogenic Common cause of infant diarrhea Non-bloody stool – watery Fever

EAggEc – Enteroaggregative Persistent watery diarrhea Lasts longer b/c aggregates together

DAEC – Diffuseaggregative Watery diarrhea Last longer b/c aggregates Bacteria are embedded in cell membrane of elongated microvilli

EHEC - Enterohemorrhagic M/C strain causing disease in developed nations Cause of “Hamburger disease” And HUS (Hemolytic Uremic Syndrome) Very low inoculation is needed (100 bacilli) Virulence Factor: Hemolysin Sx Bloody diarrhea b/c hemoragic No fever Can progress to HUS Spread via beef or other meat, feces contaminated water

HUS – Hemolytic Uremic Syndroms M/C cause of acute renal failure in children – destruction of renal glomeruli Bloody diarrhea Stool culture (+) for E. Coli Hemolytic anemia Thrombocytopenia – platelets in low number


Bacteria Salmonella

Properties Gram (-) bacillus Outer membrane – susceptible to drying – need moist surface S. Enteritidis: -Poultry, birds, reptiles -Undercooked poultry, contaminated cutting boards, egg salad, undercooked/raw eggs -High inoculum needed S. Typhi: -Foreign Travel -Spread by food or water contaminated by infected food handlers -Only small inoculum is needed

Virulence Factors Surface Antigens: -Species specific fimbria attach to M cells of Peyer’s patches – membrane ruffling: get in w/o disrupting cell membrane Invasiveness: -Penetrate into subepithelial spaces w/o a toxin mediated process -Rearrange host cell actin (membrane ruffling) Entertoxins: -LT/ST like toxins (like E. Coli) -cell associated toxin (verotoxin like) -heat labile -stabile toxins

Syndromes Salmonellosis – same syndrome whether enteritidis or typhi S. Enteritidis Gastroenteritis -6-48 hrs after ingestion of contaminated food or water -non-bloody diarrhea -fever -in and out quickly Septicemia -10% of patients develop arthritis, osteomyelitis and endocarditis Enteric Fever = Typhoid Fever -M/C spread is by food handlers infected -Unlike other salmonellosis, bacteria pass directly through intestinal walls -low inoculum **This is not Typhus** S & Sx -increasing remittent fever (comes and goes) -Rose coloured spots on abdomen – self limiting, but only in 50% of Pxs) S. Typhi Pathogenisis -replicate in GB -back into the intestine to cause increased inflammation -1-3% become chronic carriers Causes Shigellosis S. Flexneri – developing nations S. Sonnei – industrialized (milder) GI symptoms are caused by Shiga toxin Presents initially: -profuse watery diarrhea -fever Proceeds to: -abundant blood and pus in stool -tenesmus – cramping in lower abdominal; persistent ineffectual spasms; wanting to go but can’t

Other Spread by 5 Fs: Food, Fingers, Fomites, Feces, Flies -avoid antacids – b/c stomach acid will kill them if properly high -clean cutting boards

Shigella Kiosho Shiga Enterobacteriacae Related to E. Coli

Gram (-) rod Significant outer membrane Does not ferment glucose (DDX: E. Coli will ferment gluose) Very low inoculum (10-100 bacilli)

M cells in Peyer’s patches, membrane ruffling (like salmonella) Shiga exotoxin – disrupt protein synthesis Can proceed to damage glomerular epithelial cells (HUS) - like E. Coli EHEC

Fecal-oral transmission Resistant to stomach acid (unlike Salmonella) – why it only needs a small dose High likelihood of ABC resistance


No Vomiting (unlike salmonella)

200 Serotypes: EI Tor (named after camp on the way to Meca) biotype is M/C in world today Bacteria Properties Virulence Factors Vibrioacae Family Gram (-) bacillus Comma shaped Motile – single polar flagella Wide Temp Range – 18-37°C Most need salt for growth (exception is V. Cholera) Survives salt water Heat stabile High infectious dose Rarely seen in Gram stained stool or wound specimens – there are lots of them but are really small Dark field/phase contrast microscopy: characteristic darting motility (flagella) Direct ELIZA Syndromes Other

Vibrio Cholera Ubiquitous

Cholera toxin complex A-B toxin: -structurally & functionally similar to heat labil enterotoxin A of E. Coli A toxin: -increase cAMP -cause electrolye shift, watery diarrhea (can lost 1 L of water/hour) Different A-B to Cornybacterium Adhesins Mucinase

Cholera: -abrupt onset of watery diarrhea and vomiting -no abdominal cramps, no fever (unlike Shigella, Salmonella, Campylobactor) -can resemble ETEC induced gastroenteritis -Rice Water stools – no protein, speckled with mucous, colourless, odourless -Severe fluid and electrolye loss -Hypolovemic shock -Death

Shellfish/seawater is most common way to transmit (also passes Hep A) Returning Travellers – 1,000,000 cases/year in world Aggressive fluid/electrolyte replacement (oral/IV) – don’t do too quickly as osmolarity is important No long term human carriers (unlike S. Typhi)


Bacteria Bacillaceae Family Properties Gram (+) Bacillus Endospore forming – does under adverse conditions -multi-layered coat, therefore hard to get rid of Clinical samples – single or paired “jointed bamboo-rod” Culture – “Medusa head”; long, serpentine chains Resevoir: Domestic herbivores: sheep, goats, cattle, horses Virulence Factors Syndromes Other

B. Anthracis

Capsule: Anti-capsular Abs are NOT protective Normally develop Abs to a bacterial capsule that will protect you – not anthracis Toxin: 3 parts (need 2): 1. protective Ag – required for binding 2. lethal factor 3. Edema factor – adenyly cyclase

1. Cutaneous Anthrax (most common) Inoculation of skin (break in skin) – post contact with infected animals 20% mortality Mail carrier Painless, itchy, necrotic eschars (scabs) Not contagious Internal Hemorrhage Cutaneous VS Orf Bacillis Anthracus Pox Virus Spore contaminated Infected sheep or animals/products goats Painless papule Painless vesicles Necrotic escharRed weeping gelatinous edema nodules Potentially fatal (20%) Benign-self limiting 2. Inhalation Anthrax Inhalation of spores/wool – “Woolsorter’s disease”; 95% mortality -prolonged latency Initial disease goes away Comes back in Second stage: -massive enlargement of mediastinal LNs (on sternum), Hemorrhagic Meningitis Sxs M/C than pulmonary Sxs *no person to person transmission b/c no cough 3. Ingestion Anthrax Ingestions of Contaminated Food – 100% mortality IFF Upper GI: Oral/esophogeal ulcers, edema, sepsis, regional lymphadenopathy-dysphagia IFF Lower GI: n/v, malaise, systemic S & Sx, bloody diarrhea 2 types of Gastroentertitis:

Developing Countries: Endemic – can’t vaccinate all livestock Developed Countries: Occupational disease Biological warfare Prevention: Difficult due to long lived spores No person to person transmission with inhalation or ingestion anthrax

B. Cereus

Heat stable Enterotoxin:

Low mortality compared to B.



-causes emesis -found in improperly refrigerated rice dishes Heat Labile Enterotoxin: -similar to enterotoxin of ETEC and V. Cholera -causes profuse, watery diarrhea -found in contaminated meat, vegetables, sauces Cereolysin: Eye damage Phoepholipase C: Eye damage Necrotic Toxin: Eye damage

Anthracis 1. Emetic disease (vomiting) -heat stable enterotoxin -15 min to 4 hr incubation (quick incubation therefore pre-formed toxin) -no fever -no diarrhea 2. Diarrhoeal disease -heat labile enterotoxin -bloody diarrhea -no fever Also causes panopthalmitis (entire eye inflamed; recall contact lens wearers with pseudomonas) Panopthalmitis -post traumatic -Rapid (<48 hrs) Exam Q: What would happen if you heated rice? Treatment/Prevention: Gastroenteritis: -rapid consumption of food after eating -proper refrigeration of uneaten portions no ABCs – is already a toxin when in the food Panopthalmitis: Early, aggressive ABCs

Clostridium Spp. C. Perfringen Histotoxic

Gram (+) bacilli *M/C’ly anaerobic *Spore formers Gram (+) Plump, rectangular rod (Sausage) Non-motile but rapid growth on sheep’s blood agar (divide in 15-18mins) Ubiquitous – opportunistic: Soil, GIT of animals and humans, contaminated water

5 toxin specific types: Type A: Permanent soil inhabitant, responsible for most human disease Spore Formation Toxin Formation: Alpha toxin: Most tissue damage – increase vascular permeability (lyse cells) Disease M/C after trauma that causes ischemia: -Needs devitalized tissue (more acidic) -Favours lowered pO2 and pH

Wound/soft tissue infections Anaerobic cellulites (as with Strep): • • • • organism spread through subcutaneous tissue spares fascia and deep muscle superficial skin discoloration and skin necrosis gas forms – develop suppurative myositis – foul smelling discharge no muscle necrosis, no systemic Ss and Sxs (DDX from myonecrosis)

Lots in wounds and times of war and car accidents etc. If mm doesn’t respons to stimulus = gas gangrene (myonecrosis) If does respond = still cellulites (take skin of to test mm and see) Food Poisoning M/C: 1. Campylobacter 2. Salmonella 3. Staph Aureus 4. C. Perfringens

Myonecrosis (Gas Gangrene) • Rapid worsening of cellulites • Rapid onset of intense pain • Extensive muscle necrosis (blue black, edematous, does not bleed or contract on stimulation) • Toxic delirium


• • • •

Much damage due to alpha toxin and gas bubbles (bubble pack material crepitis – cracking sound from gas bubbles) Debridement and examination of underlying muscle tissue Fast growth of culture of sheep’s blood agar Nagler’s reaction Gram(+) rods in tissue specimens with no leukocytes

C. Difficile Enterotoxigenic

Toxin A (Entertoxin): • Hemorrhagic necrosis in pseudo membranous colitis Hyaluronidase: • Increase spread between tissues

Food Poisoning • Ingest meat – refrigeration and re-heating destroys entertoxins • Large infection dose • Abdominal cramps • Watery diarrhea • No fever • No N/V • Looks similar to salmonella Range of Problems: • Mild Diarhea • Colitis • Life threatening pseudo membranous colitis • Prolonged diarrhea (signs of dehydration) Pseudo Membranous colitis • is confirmed by biopsy – multiple, raised white/yellow exudative plaques adhering to colonic mucosa • in vitro cytotoxicity assay in culture cells

Can be normal part of GI flora W/O causing disease M/C causes post-ABC diarrhea and pseudo membranous colitis (also caused by Staph Aureus) M/C ly after broad spectrum ABCs Treatment: • Discontinue ABCs • Maintina fluid/electrolyte balands • Avoid drug therapies that decrease intestinal motility Prevent By: • Prescribe ABCs with probiotics (separate by 8hrs)

• •

immunoassay for C. Difficile toxins A and B (look for toxins using Direct ELISA); best way to diagnose Sigmoidoscopy Fecal leukocytes


C. Tetani Paralytic Clostridium = cloister (of nuns), spindle Tetani = extreme tension

Gram stain variable (-) when old (+) when fresh Looks like a tennis racquet • Very sensitive to O2 obligate anaerobe Relatively inactive metabolically (unlike C. Perfringen)

Spores: Survive adverse conditions Have to boil for 3 hours Tetanospasmin: • Heat labile neurotoxin (one of three most potent toxins) • Responsible for the spastic paralysis • 2 part toxin – postsynaptic terminals in CNS; irreversibly inhibits the release of GABA and glycine Ubiquitous – spores last for years in soil Present in GIT of cows, horses and some humans

4 types of Tetanus – Generalized, localized, cephalic, neonatal Generalized Tetanus • M/C form of tetanus • Bacterium introduced by trauma to skin • Animal bites S and Sxs: • Exaggerated DTRs (reflexes) • Trismus (lock jaw) • Risus Sardonicus (mocking smile) • Drooling • Opisthotonus (paraspinal muscles arch backwards) happens later Neonatal • From improperly cleaned umbilical stupm • First sign is difficulty sucking (8-19 days after birth)

Developed world: • Low disease incidence – immunization, herd immunity, urbanization Developing world: • Higher • Infant tetanus can be a problem (>50% of neonatal deaths) Diagnosis • Patient history • Clinical S and Sxs

Gram stain and culture not that important (only 30% of people with tetanus are culture (+))

Treatment • Tetanospasmin binds irreversibly and therefore, can only treat symptoms until nerve terminals regenerate • Passive immunization – bind free tetanospasmin Prevention • No natural immunity unlike many other disease • Active immunization – tetanus toxoids: booster every 10 years


C. Botilinum Paralytic

Gran (+) bacillus Sausage shaped Produces one of the most potent exotoxins known to humans – lethal dose < 1ug Ubiquitous – soil, sediments of lakes and ponds

Spore Formation: One of the most resistant: • Heat (hrs at 100C and 10 mins at 120C) • Cold (down to -190C)

Intoxication (toxin, not bacteria)– Food borne botulism Inadequate sterilization of food (home canned foods – beans, asparagus b/c low acidity, preserved fish) S and Sx • 2-72 hour incubation • No GI distress unlike other food poisonings • No fever

Too much Mg can mimic botulism Diagnosis: Clinical signs and symptoms are paramount Prevention: • Acid pH (canned fruit is ok) – grow best at pH>4.5 • Refrigerate (can’t survive <4C) • Heat for minimum 20 min at 80C • No honey to infants < 1yoa • Check cans – contaminated ones might be swollen from gas released by bacterial enzymes)


VERY RESISTENT Botulinum Toxin • One of the most potent known neurotoxins • Cholinergic neurons

• • • •

Inhibits acetylcholine release at presynaptic terminals and therefore flaccid paralysis (opposite to tetanospasmin) (don’t get excitatory signal)

Clear sensorium (thinking) – completely aware Dilated, fixed pupils when eye is exposed to light source - bilateral Dry, fuzzy tongue – Furry tongue, red, dry Bilateral descending weakness of neck, face, throat Respiratory paralysis – mortality (32-40%)

No permanent immunity – can get repeated occurrences Infant Botulism – Infection Intoxication • Honey contaminated with spores • M/C form of botulism in USA • M/C in 1-6 months old because caused by bacteria growing and producing neurotoxin in infant GIT; infant GIT doesn’t have as many competitive bowel microbes S and Sx • Non-specific • Floppy baby


Bacteria Campylobacter Properties Gran (-) bacillus “S or gull-wing shaped” Small (0.3-0.6um) Filterable unlike other bacteria – will go through a filter, other bacteria are too big Motile Single polar flagella Microaerophilic reduced O2, increased CO2) Thermophilic (42°C)(needs higher temp than others) C. Jejuni Gastroenteritis: Need high infectious dose (need reduced with hypochlorhydria (elderly; parietal cells get hammered), TUMs (buffered; many elderly given to get Ca – not good system b/c Cl to bind Ca & if lowered HCL via TUMs won’t work), milk 2-11 day incubation foul smelling, watery diarrhea progressing to profuse bloody diarrhea. No vomiting Resolutiong in 3 days to 3 weeks Residual histological damage (effect absorption) Guillain Barre Syndrome: -idiopathic, peripheral polyneuritis 1-3 weeks after the mild condition -progressive, symmetric pain and weakness in extremities – might ascend to trunk, face, thorax -attack myelin of nerves, get symmetrical weakness -auto-immune link -self-limiting (few weeks to months) with 3 most common ways to get diarrhea: 1. Campylobacter Jejuni 2. Enterotoxigenic E. Coli 3. Rhodovirus #1 bacterial cause of gastroenteritis and endocarditis in USA Treatment/Prevention : Gastroenteritis: -prevent with proper preparation and storage of food -avoid raw milk proper water treatment Guillain Barre Syndrome: No treatment Virulence Factors Syndromes Other Zoonoses: birds Raw milk and water Peak incidence in young adults (20-29 yoa)


Bacteria Helicobacter pylori Like Campylobacter In it’s own family

Properties Gram stain variable – changes depending on age of culture Corkscrew motion – highly motile Urease (+) (alkaline buffer; cloud of ammonia around them from breaking down urea Very slow growth (2-6 day) in complex media Temp 30-37C (not at 42C like Campylobacter Until early 80s thought that stomach acid was too low to grow – wrong Stomach of humans, primate, pigs, cheetahs, dogs, ferrets, mice, rats (but they don’t all get gastritis) Found in gastric antrum and body only (not in fundus or pyloric region) Developed countries – up to 45% in adults > 50 yoa

Virulence Factors Survive Acidity: -acid inhibitory protein (blocks release of acid from parietal cells) -Urease Flagella Mucinase/phospholipase (enzymes break up stomach lining so it can get through) Microaerophilic: -survive relatively anaerobic environment of ST Tissue Damaging: PAF – hypersecretion of gastric acid

complete recovery Syndromes Type B (infective) gastritis) -30-50% of people with gastritis have H. Pylori but M/C asymptomatic S & Sx & Lab Dx -Epigastric pain -Foul smelling breath -13C urea breath test -anti H. Pylori Abs (IgG) -gastroscopy with biopsy -CLO test (+) – Campylobacter-like organ test Progresses to: PUD; especially duodenal ulcers S & Sx & Lab Dx • burning, gnawing upper GI pain 1-3 hours after meals, • worse night

Other Stress → ↑acidity → ↑ H. Pylori Possibly spread through dental plague and saliva, but don’t really know Increased risk with pickley foods, salted fish and meats, smoked meats

• • •

better eating or antacids (best with protein b/c good buffer) Endoscopy Urea breath test Serology (anti-H. Pylori Abs)

< 20% of people, regardless of age, who test + for H. Pylori also get Peptic Ulcer Disease (PUD)

Gastric Adenocarcinmo -sequelae of untreated chronic gastritis classified as a Class I carcinogen S & Sx • Fatigue • Weight loss • Low grade fever • Night pain • Hemoccult (+) stools • Anemia M/C cancer in the world behind Lung Gastric mucosa-associated lymphoid type (MALT) B cell lymphomas Rare No evidence that eradicating H. Pylori prevents progression of gastritis to

Treatment: Gastric mucosa-associated lymphoid type (MALT) B cell lymphomas Triple Therapy: Proton pump inhibitor (omeprazole), clarithromycin, metronidazole, bismuth 2 week course gets rid of 90% of H. Pylori



Bacteria Neisseria Spp Properties Gram(-) diplococci “coffee bean” transparent, nonpigmented colonies on chocolate blood agar (heat treated blood agar) Normal colonizer of nasopharynx or cause disease (opportunistic) Virulence Factors Syndromes Other

N. Meningitidis

Pili – needed to attach to non-ciliated columnar cells Bacteria enters host cell and replicates in phagocytic vacules Capsule is also antiphagocytic LOS expressed?

Asymptomatically colonize nasopharynx or cause meningitis, meningococcemia or pneumonia M/C cause of bacterial meningitis in infants through adolescence and in young adults Transferred via close contact with respiratory droplets (day cares, military barracks) Meningococcemia (Mild disease) • Arthritis

Meningitis Causes: 1. N. Meningitides 2. H. influenza 3. S. pneumonia

Petechial skin rashes (little red dots)

Meningicoccemia (marked disease) • URI then 1-3 day incubation • Small petechial rash on trunk and lower extremities that can coalesce to form larger bullae (due to thrombosis of small blood vessels) Meningococcal meningitis • 2nd most common cause of adult bacterial meningitis • 1st is strep pneumonia • rapid onset of fever, nuchal rigidity, blinding headache • high number of organisms • Gram (-) diplococci in PMNs


N. Gonorrhoeae

Gram(-) diplococci On chocolate blood agar Strict pathogen “the gonococcus” fastidious growth – no growth with drying therefore has to stay moist, therefore needs intimate sexual contact Gram stain is sensitive and specific IFF men with purulent urethritis – doesn’t work for women For women, must confirm with culture

No exotoxin: • Host damage is from gonococcal induced inflammatory response Pili: • Non-ciliated epithelial cells of foreskin, vagina, fallopian tube • Highly variable structure; therefore can get gonorrhoea more than once LOS (Lipo Oligo Saccharide): • Classic endotoxin activity (like LPS) • No strain specific O antigens (unlike LPS) IgA protease

95% of males get acut symptoms: • gonococcal urethritis 2-7 day incubation: • purulent urethral discharge

2nd most common STD in US Chlamydia is #1 M/C in 15-24 yoa Increased risk if: • Female (50% risk with single exposure as opposed to males with 20% risk) • multiple sex partners Women are M/C’ly asymptomatic carriers – don’t know they have disease until try to have kids and find out they are infertile because scarring has blocked their fallopian tubes. -associated with Chlamydia -stays on foreskin, therefore less risk is circumsized Penicillin resistant – betalactamase, need too high dose, change cell surface so ABC can’t penetrate cell

red/edematous urethral meatus (opening at end of penis)

>50% of women are asymptomatic or mild symptoms: • cervicitis • vaginal discharge • abnormal vaginal bleeding • ascending infection • major cause of infertility Disseminated Gonorrhoea • Rare but M/C in women (1-3%) • Migratory arthralgias • Tender papillary lesions • Rash on the extremeties • Arthritis – M/C ly mono articular knee in females N. Gonorrhoea is the #1 cause of purulent (pussy) arthritis in young adults Opthalmia Neonatorum • Caused by N. gonorrhoea of C. trachomatis • Purulent conjunctivitis in newborns infected during vaginal delivery • Sticky discharge • Edema / inflammation *know what bacteria effect the eyes*


Bacteria Haemophilus Spp = “blood loving”

Properties Small Gram (-) Coccobacillus (pleomorphic) Fastidious growth requirements: X factor (hematin) and V factor (NAD) Chocolate agar Obligate parasites on mucous membranes of humans and animals

Virulence Factors


Other 1st to have whole genome sequenced

H. influenzae

Chocolate Agar Conjugated HiB vaccine (purified PRP)

Non-encapsulated strains – colonize both upper and lower respiratory tracts Encapsulated strains (serotype b) – can become systemic Capsule: Invasive disease is M/C’ly due to H. influenzae type b (“Hib” infection) Pili: Damage respiratory, ciliated epithelium LPS: Responsible for meningitis

Pneumonia Meningitis • Same S and Sx as other bacterial meningitis • But more insidious onet and increased risk of neurological sequelae • Used to be most common cause of meningitis before vaccine • Lots of kids get, but few die Epiglottitis • Medical emergency (can’t breath( • M/C in boys 2-4 yoa • Dysphagia • Drooling • Muffled voice • Minimal cough • Severs dyspnea

25-80% of us have nonencapsulated form in us all the time Primarily a paediatric problem (< 2yoa at very high risk) b/c can’t block capsule

Vaccine will not stop OM, OS or pneumonia b/c caused by nonencapsulated strains and vaccine works against capsule Vaccine works against meningitis

Don’t want to swab when extremely inflamed – painful

Otitis Media/Sinusitis M/C caused by: 1. H. influenzae 2. S. Pneumonia 3. Moraxella catarrhalis


H. Ducreyi

Small Gram (-) Coccobacillus Non-encapsulated Aka Ducreyi bacillus

Can cause an STD – M/Cly in developing world • • Causes chancroid (soft chancre) Unlike primary syphilis which causes hard chancre Chancroid H. Ducreyi Soft, purulent, painful ulcer on genitalia M/C in males, uncircumcised, tropical & sub-tropical Females M/C asymptomatis 5-7 day incubation Progress to painful buboes, phimosis (can’t retract foreskin), urethral stricture Gram(-) coccobacillur Primary syphilis Treponema pallidum Hard, non-purulent, nonpainful ulcer (genitalia, anus, mouth) Both sexes 20-35 yoa 3 week incubation Painless buboes

Perhaps isn’t Haemophillus – wrongly named?

Poor Gram stain: Dark field microscopy (spiral rods, thin, tightly coiled), non-specific tests (VRDL, RPR), specific tests (FTA-Abs, TPHA)


Bacteria Bordetella Spp

Properties Gram (-) Very small bacilli (rodlike) Fastidious (picky) growth Needs humidity, specialized media (charcoal, blood, NADenriched) Haemophilus also needs chocolate agar

Virulence Factors

Syndromes Bordetella Pertussis (whooping cough)

Other Pertussis vaccine now found to only last for 10 years. Want people to pay to get booster, but only a mild disease in adults.

Bordetella Pertussis

Bacteria is best isolated using nasopharyngeal aspirates during catarrhal stage Culture – difficult because need humidity, 35C, 7days, specialized agar. Only 50% of infected people are culture (+)

Pertussis toxin: • Increase adenylate cyclase • cAMP – respiratory secretions/mucous Tracheal Cytotoxin: • Part of the PG layer • Cause ciliostatis and then damage to ciliated epithelial cells • Causes cough • Can’t repair damaged cells due to DNA interference • Increase IL-1 causes fever Filamentous Haemagglutin and other adhesions: • Intracellular survival protects against clearance by humoral immunity

Whooping Cough (4 stages) 1. Incubation – 7-10 days, sub-clinical (no Sxs), increasing # of bacteria

Reportable Disease M/C in developing countries in children < 1yoa Spread by infectious droplets No long term immunity “protection” in developed countries due to DPT vaccine no environmental or animal reservoir known Treatment and Prevention: ABCs are of limited use (disease is not recognized until peak of infectiousness has passed.) ABCs are meant for when bacteria is actively dividing. DPT vaccine – 2, 4, 6, 15 months and 4-6 years Used to use whole cell vaccine (DTwP) – caused side effects No use acllular B. Pertussis (DTaP) which causes “fewer

2. Catarrhal – 2 weeks, looks like common
cold, rhinorrhea. Most infectious stage. Peak number of bacteria

3. Paroxysmal stage – 1-2 weeks, dry nonproductive, repetitive “whooping” cough. 40-50 coughs/day causing damage and exhaustion

4. Convalescent Stage – 2-4 weeks.
Cough resolves but can have secondary complications. Hard to DDX because looks like a cold in Catarrhal stage which is when it should be treated because damage isn’t done yet and is highest bacterial count. Usually DX at Paroxysmal stage when bacteria have moved into the cells. Coughing can collapse lung, cause hernia


side effects”

Bacteria Treponema Pallidum Properties Small Thin Coiled spirochetes Can’t usually visualize via gram stain and light microscopy Only in cultured rabbit epithelial cells Humans are the only reservoir of disease Susceptible to drying (like niesseria), therefore can’t get from toilet seat Contagious only during primary stage and rash of secondary stage Syphilis lab diagnosis: • No gram stain b/c too small • Use silver or fluorescent stains Virulence Factors Motile – corkscrew motility via thin fibrils at both ends, but no flagella Syndromes 3 different Subspecies Cause: Syphillus, Bjel, and Pinta Strict Human Pathogen Other

Treponema Pallidum subspecies pallidum

Outer membrane: • Proteins to adhere to host cell – covers itself with host cell protein Very labile

Syphilis Primary: • Small papule – painless, hard chancre (VS H. Ducreyi) • Painless, regional lymphadenopathybuboes • Very infectious • Heals spontaneously within 2 months without scarring Secondary: • Flu-like syndrome • Localized lymphadenopathy

3rd M/C bacterial STD in the USA 1. Chlamydia 2. Gonorrhoea 3. Syphilis Syphilis Treatment and prevention: • Hygiene (spirochetes destroyed by soap and water, temperature >42C and drying • Safe sex practices

• •

Non-specific tests: VDRL (Venereal Disease Research Laboratory test) and RPR Indicate current active disease Specific tests: FTA (fluorescent Tremanemal A?) and TPHA (MHA-TP) Indicate past infection

• • • •

Diffuse, non-pruritic maculopapular rash – wide spread even on palms • Very infectious (kissing) • Resolves slowly in weeks to months Tertiary (Lues/Leutic): • After 3-40 years of latent syphilis o Long latent people where not contagious. Causing tumors but don’t know until see S & Sx later on • Gummmas – rubbery tumor • Can effect many organ systems: o Neurosyphilis o Cardiosyphilis • Painless or deep burrowing pain Congenital Syphilis (vertical transmission) • Infected mother infects fetus


Only primary ad secondary stage syphilis can be found in tests

Born appearing well then several weeks or up to 2 years later get snuffles (bloody nasal discharge), widespread desquamating maculopapular rash

Bacteria Chlamydophila C. Psittaci C. pneumonia C. Trachomatis Properties VERY Small Gram (-) (very weak though) Bacillus Virus like properties Unlike other bacteria there is not PG layer, therefore no Gram stain Unique growth cycle within host cell – EBs and RBs Virulence Factors • Gains access through minute abrasions or laverations • Limited tissue tropism Strains causing LGV can cause systemic infections by entering lymphatic system Clinical signs and symptoms due to direct destruction of cells during replication ad host inflammatory response No long term immunity Syndromes Chlamydia growth cycle: Elementary body: Adapted for extracellular survival and initiation of infection (resistant to environment) Reticulate Body: Adapted for intracellular growth; metabolically active (growth phase) Inclusion Body: High amount of glycogen, therefore stain with iodine. Trachoma • Leading cause of preventable blindness in developing countries • M/C in children • Poor hygiene • M/Cly spread by droplets, hands, contaminated clothing, eye make-up, flies • • Could decrease by 50% if had enough water to wash just once per day Must have specific attachment to conjunctiva Resist flushing from tears – sticks to eye Begins as conjunctivitis Inflamed eyelids cause entropion (eyelashes chronically irritate cornea cause ulceration Other Can get from toilet seat Chlamydia Urogenital Infections Currently M/C bacterial STD in USA Women: • Termed Chlamydia (the Clap) • M/C asymptomatic (80%) • Pain/cramping in lower abdomen • Dyspaerunia • Bleeding between menses Men • Termed NGU (non gonoccocal urethritis) • M/Cly symptomatic (75%) • Yellow clear discharge • Pain, tenderness of genitals • Reactive arthritis (Reiter’s syndrome) Reactive Arthritis (Reiter’s syndrome) • Seronegative spondyloarthropathy • M/C in young men (2040yoa) • That are HLA-B27 positive • C. Trachomatis in M/C bacterial pathogen

Trachoma inclusion conjunctivitis Adult: M/Cly 18-30 yoa and sexually active Genital infection 1st and then unilateral mucopurulent discharge in eye


Neonatal: Bilateral, intense papillary conjunctivitis with lid swelling Lymphogranuloma venereum (LGV) • M/C in Africa, Asia, South America • M/C in male homosexuals Initial lesion: • Small painless papule on penis, urethra, glans, scrotum and vaginal wall (similar to Syphilis but not a chancre) 2nd Stage: • inflammation and swelling in LNs (buboes) – painful, can rupture and drain spontaneously • systemic • can get proctitis in men and women C. Trachomatis Lab Dx: Need adequate sample of infected cells (specimen of pus/discharge is inappropriate) – b/c bacteria are intracellular so do scraping Culture: • most specific method • only infects certain cell lines • formation of inclusion bodies (key to recognizing) C. pheumonia Human pathogen that can cause atypical pneumonia (mild/persistent cough and malaise that might progress to lobar pneumonia) Potential link to atherosclerosis, MS, Alzheimer’s? Causes psittacosis • Biggest risk from psittacine birds (parrots, macawsm parakeets, cockatiels)

• •

Unexplained diarrhea Superficial lesions on palms/sole/oral mucosa

“Can’t see, can’t pee, can’t dance with me”
Treatment: • M/C also have presumptive Tx for Gonorrhea Prevention: • Hygiene (hand/face washing) • Practise safe sex

C. psittaci


• • • • Bacteria Mycobacterium Spp. M. tuberculosis M. Leprae M. avium Complex M. Gordonae Properties Acid Fast Gram (+) Bacillus One of the slower dividing microorganisms – 12-24 hours Mycolic acid in its cell wall Acid fast Resist drying, detergents, acids/bases Source of PPD for Mantoux test Looks kinda like a fungus in culture Cause of more fatalities worldwide than any other infectious disease M/C’ly person to person transmission via infectious aerosolized particles Very small inoculum needed Immunocompromised have increased risk Sputum Sample: • Acid fast bacillus • Fluorescent stain • Fastidious culture requirements Virulence Factors

Transmitted via inhaled dried bird excrement, urine and respiratory secretions Non-productive cough Commonly progresses to CNS 5% mortality



M. tuberculosis

Evade humoral immunity because intracellular growth Tissue destruction is due primarily to host immune response Form tubercles – body reacts to contain bacteria by enclosing in small, fibrous granulomas containing epithelial cells and Giant (Langehan) cells – develop to larger necrotic or caseous granulomas

Pulmonary TB Primary Infection: • Only 5% get active TB within 2 years of exposure • Ghon complex – initial lung lesion and locally enlarged LNs Insidious onset • Malaise/listlessness • Night sweats • Low grade fever • Unexplained weight loss • Progressive fatigue CXR: Cavitations in one or more upper lobes of lung Miliary TB • No pulmonary sign

On the rise in North America – 1 new person infected every second “TB is the master impersonator” Treatment: • Problem – MDR-TB Prevention: • Diet/robust immune system • Only 5% of all vaccine preventable deaths are due to TB



Skin test (Mantoux test): • Wait 48 hours and measure induration/ erythema M. Leprae Similar structure to M. tuberculosis but: Can not be artificially cultured (need live mice or armadillos) and grow in Globi bundles (encapsulated globs of rods in tissues) Armadillos are naturally infected and provide a natural reservoir for disease Spread via respiratory route or contact with break in skin M. avium Complex MAC Similar to tuberculosis but only causes opportunistic infections • • • Disease in HIV/AIDs patients Lymphadenitis in children Ubiquitous in water Capsule Preference for lower temperatures – limits infection to skin and nasopharynx Intracellular survival – in Histiocytes and Schwann cells

• •

Effects the liver and others Tubercle resembles millet seed

Tuberculoid (Paucibacillary) • Pauca = few • Not infectious • <5 cutaneous macular lesions with hypopigmented centers • will react to skin test – lepromin Lepromatous (Multibacillary) • Highly infectious

Most destructive – disfiguring skin/bone, cartilage lesions (“Leonine faces”) • Anhidrosis (deficiency or absence of sweating) • Not reactive to skin test (Leprumanin test) • >5 skin lesions • tend to get with weak cellular immunity but strong humoral immunity Begins as mild pulmonary disease and spread to local lymph nodes and then quickly to every organ Pulmonary disease is similar to TB: • Usually GIT tract involvement • Usually fatal within months No person to person spread via aerosolized droplet Mostly obtained by ingestion

Over half the people in USA with HIV/AIDs also have MAC Increased risk in elderly women in lingual of lung – Lady Windermere Syndrome


Bacteria Borrelia Spp.

Properties Gram (-) Spirochete Larger than other spirochetes and more complex Many species cause relapsing fever and Lyme disease (Borellia burgdorferi) – need ticks as vectors

Virulence Factors



B. burgdorferi

M/C vector borne disease in USA No person to person spread Vector: deer tick (Ioxdes scapularis/Ioxdes pacificus) Resevoir: White footed mouse or white tailed deer Increased risk in grassy, wooded areas

Lyme Disease Stage One (of 3): Erythema migrans rash “bull’s eye lesions” Diagnosis: • Clinical signs and Sxs and patient history • Culture and IFA stain of biopsy of initial rash • Indirect ELISA


Bacteria Leptospira Spp

Properties Spirochete Minimal nutrition requirements (LCFA, vitamin B1 and B12) Survive in moist, slightly alkaline environment for many days

Virulence Factors Spirochete enters via contaminated urine – entry to broken skin and mucosa Replicate in endothelium lining of capillaries Significant cause of KI failure


Other Zoonotic – rodent and domestic dog reservoirs M/C’ly acquire disease via contact with infected urine

L. interrogenes

Human pathogen Leptospirosis No skin lesion at site of entry (unlike Lyme disease) • Septic Phase o Abrupt onset fever, severe H/A, severe myalgia (esp. calf and back), nausea o Lasts 1 week Immune Phase o 2 days asymptomatic, then aseptic meningitis with severe H/A, N/V, myalgia Weil’s disease (icteric = jaundice) o KI failure (M/C cause of death)

Lab Dx Too small for light microscope and Gram stain


Bacteria Rickettsia Spp

Properties Energy parasite – like Chlamydia needs energy from host Small bacteria Similar to Gram (-) bacteria No flagella

Virulence Factors Tick bite – must be exposed to tick for >24hrs Tissue damage due to multiplication in vascular epithelium damaging cells causing leakage … organ failure


Other Need arthropod vectors – hard ticks like dog tick (Dermacenter variabili) Need tick like Lyme Disease

R. ricketsii

Rocky Mountain Spotted Fever Painless tick bite leaves no mwar (very low inoculum <10 organisms) 1 week incubation 5 days later rash – diffuse, maculopapular rash, M/C spread from extremities to trunk (including palms and soles) Typhoid Salmonella typhi Transmitted by contaminated milk, water, food Typhus Rickettsia ricketsii Transmitted from infected rodents to humans by bites of ticks, lice, fleas or mites Rash Blanching Erythema chronicum migrans Faint macuopapular Maculopapular rosy spots over skin eschar formation. of abdomen and chest Not on face, soles, palms

RMSF Lad Dx: DFA (Direct Flourescent Ab) stain Prevention Almost impossible to get rid of ticks – can surviv up to 4 years without feeding


Hard to treat because are eukaryotes therefore look like us and any treatment will also effect us – serious side effects. Monomorphic or Dimorphic depending on species – more are Di Dimorphic means are a different structure in the environment to in the body because of change in temperature Filamentous: • Molds • M/C at lower temperature and free living Unicellular • Yeasts • M/C at higher temperature and when parasitizing tissue (in you) Fungal Disease Classification: 1. Superficial ⇒ Infect only outermost layers of skin and hair

⇒ eg - Black and white piedre, tinea versicolor, tinea nigra 2. Cutaneous ⇒ Most tineas ⇒ Most infectious disease – ring worm 3. Submucotaneous 4. Systemic ⇒ Invade internal organ M/C’ly from lung foci of infection 
Histoplasmosis, blastomycosis, coccidioidomycoses


Fungal Type Superficial Mycoses

Properties Outermost, non-living layer of skin (survive by diffusion) No immune reaction because no blood or langerhan cells Primarily cosmetic issues only

Virulence Factors

Syndromes Tinea (pityriasis) versicolor (bran like) • Malassezia furfur • Non-itchy hypo-pigmented lesions on upper torso, arms, abdomen • Dandruff like • Concentrate near sebaceous gland 0 axilla • “spaghetti and meatballs” organism after KOH preparation • Wood’s lamp (+) (will fluoresce) Tinea Nigra • Found in soil

Other Tinea = worm/moth like

Macular lesions on palms and soles Dark pigmented yeast cells

Black Piedra • Black under microscope • Dark, hard nodules • Hairs of scalp, moustache, beard • Direct or sexual contact • Gritty feeling when combing hair • Alopecia possible • Really notice under microscope White Piedra • Soft, pasty white • Direct contact only Cutaneous Mycoses From showers 2nd M/C disease in adults

Piedra = more than 2 colours

Tinea Cruris – Jock itch Tinea Pedis – Athletes foot Contagious – wear gloved

Deeper layers Evoke inflammatory immune response Clinical diseases are termed tineas (worm like lesions) Wood’s lamp (+) Mistakenly termed dermatophytes (thought was by plants, but isn’t) Further names according to what part of the body they are found


Subcutaneus Mycoses

Fascia, muscle, bone M/C’ly due to tissue trauma Difficult to treat – debridement (cutting out), amputation M/C’ly develop mild acute/ asymptomatic lung infections Also can develop chronic disease or sub-clinical (latent)

Systemic Mycoses

Monomorphic – cryptococcus neoformans Or Dimorphic – thermal dimorphism

Strict pathogens and Opportunistic pathogens Mycotic agents • Cause disease in healthy humans

Histoplasma capsulatum

Saprobic phase • In N2 rich soil (farms) Parasitic phase • In macrophages of RES M/C found in “Histo” belt Grows in soil rich in nitrogen Also in areas of a lot of bird (starling/ chicken) and bat excrement Inhale Convert to yeast form and replicate in macrophages Carried by lymphatics

Inhale Convert to yeast form and replicate in macrophages Carried by lymphatics Lab Dx Microscopy: • 10% KOH prep with Silver or Glemsa stain Serological: • Skin tests • Too many false (+) Cultures: Slow growing (1-2 weeks) and spores are infectious

Respiratory tract as initial foci of infection Primary Histoplasmosis • 10 day incubation • Flu like • Acute, self-limiting, influenza like illness • Some residual calcified lesions • Not contagious • Overly aggressive immune response • Mediastinal fibrosis

KOH gets rid of “background” noise (other cells)

Ocular histoplasmosis syndrome is a possible comlication

Ocular Histoplasmosis Syndrome • Serious retinal condition • Leading cause of blindness in 20-40 yoa • “histo spots” bilaterally – little black spots o yeast travels through blood vessels to eyes • M/C’ly no visual loss Histoplasmomis • Progressive – disseminated via lymphatics – increased risk if impaired CMI • TB-like iff chronic



Fever, night sweats, weight loss with destructive (caseating necrosis) lung lesions Know all TB like illnesses

Blastomyces Dermatides

Endemic areas overlap those of histoplasmosis Unknown reservoir – unlike H capsulatum it is rarely cultured from soil Dust clouds at construction sites or crop dust during farming Inhale condia (sexual phase of fungi) Replicate in macrophages Carried by lymphatics or blood

Lab Dx Skin test and serology • Too many false (+) Microscopy • Biopsy/ histology of KOH prepped tissue sample Culture • On selective Sabourand agar

Blastomycosis (Gilchrists disease, Chicago Disease) Acute • Bronchopneumonia • Drenching sweats

No residual calcified lesions (unlike Histoplasmosis) Not contagious even if they cough

Chronic • TB or cancer like Blastomycosis skin lesions • Slowly expanding ulcerative or verrucous (wart like) lesions • Face, nose, mouth Saprobic Form Coccidiodomycosis (San Joaquin Valley fever, desert rheumatism, Posada – Wernicke disease) Inhalation of conidia • M/C’ly asymptomatic • 40% mild, febrile to moderately severe respiratory disease • not contagious • erthyema nodosum with arthralgia (pain in joints) Dx: Skin test antigens • Use for skin test 2-4 weeks after symptoms • Coccidiodin – cell free culture of mycellum growth • Spherulin – cell free culture of spherule phase CXR “Egg shell” lesions Tissue biopsy

Coccidiodes immitis

Dimorphic 37C, tissue, multinucleated spherule “sporangia” endemic in soils of hot dry, semi-arid areas extensively spread via dusty storms M/C’ly in males 25-55 yoa

Parasitic Form


Staining and microscopy for spherules Culture • Caution – infections; leading cause of lab acquired infections


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