Micro Chart Test 2

Types

Morphology

Epidemiology

Yersinia enterolytica: forms envelope/ Gram (-) rod or coccobacillus outer membrane

Ubiquitous

Yersinia pestis: forms protein polysaccharide capsule

Bipolar staining: "safety pin" appearance

Zoonotic: most common vectors are rodents: rats, ground squirrels, rabbits, mice, prairie dogs, cats, ect.

Facultative anaerobe

Can be transmitted by:

Indole (-), catalase (+), urease (-)

1) fleas, Xenopsylla cheopsis, that feed on an infected animal and then bite humans

Yersinia spp.

5) Iron absorbance factor: independent of siderophores

4) Prophylactic ABCs to prevent high bactermia: plague is toxigenic

Grows best at 22-55 C but also grows at 4 C

6) Various exotoxins and endotoxins: Yersinia entrolytica gastroenteritis/ 5) Proper sanitation/ personal lipid A part of LPS Yersinosis hygiene 7) Protein YopJ: blocks 2 critical cellular signaling pathways and therefore Bubonic plague induces cell death

Gram (-) baccilus

Sweet, grape-like fruity odor

Cytocrome oxidase (+) and nonfermenters 3 colony types (rough, smooth, mucoid) depending on where isolated

3) direct contact on open wound on skin

1) over crowding, poor sanitation, poor personal Pneumonic plauge hygiene 2) Native Americans, hunters, hikers/campers, Septicemic plague veterinarians 3) Cold climates: Y. enterolytica. Warm/cool damp climates: Y pestis Ubiquitous - soil, water, plants, hospital sinks Infections involve: 1) attachment and and respiratory equipment, swimming pools, colonization, 2) local invasion, 3) Bacterial Keratitis raw vegetables disseminated systemic disease 1) Attachment and colonization: a) opportunistic fimbria/ pili, b) alginate slime/polysaccharide capsule (anchors UTI's Two forms: bioflim or planktonic bacteria to host cell, protect from host immunity. Increase expression if host has COPD or CF) Low incidence of normal human colonization: 2) Local invasion: elastase, pyocyanin opportunistic pathogen of humans and horses. (interfere with function of nasal cilia and GIT infections Almost never causes disease in disrupts respiratory epithelium), ABC immunocompetent host resistance Cause wide range of diseases: primary focus of infection is LU - major cause of morbidity and 3) Dissemination: LPS and exototins Swimmer's Ear mortality in CF Also cause soft tissue infections (esp after Toxigenesis: Exotoxin A: same burns) bacteremia, ear and eye infections and Bactermia mechanism of action as Diptheriae toxin systemic infections

motile with single, polar flagella (unlike proteus but like legionella)

Family Enterobacteriaceae, genus Escherichia, species E. coli

Escherichia coli

Prevention/ Treatment

Will not ferment sucrose, rhamnose, 2) Inhalation of infectious droplets cellubiose

Most common flat colonies with spreading borders, B hemolysis, green pigment

Pesudomonas areuginosa

Diseases

Yersinia pestis disease prevention:

Increased Risk with:

Not a member of the Enterobacteriaceae family

Virulence Factors

1) Invasion gene product: uptake into Yersinia enterolytica diseases epithelia cells and macrophages of PP Common cause of food borne 2) Anti phagocytic factors: a) capsular gastroenteritis in: Sandinavia, Ag; b) Type III protein secretion system Europe and colder parts of NA Major sources of contamination are: refrigerated milk products, 3) Plasminogen activator protease: cold meat (Porl), water degrades C3a and C3b contaminated with feces, blood products Animal hosts include: rodents, 4) Fribrinolysin rabbits, pigs, sheep, cattle, horses, domestic pets

Obligate aerobes (can grow anaerobically iff Arginine or nitrate source) Minimal nutritional requirements can grow in distilled water Optimal temperature growth is 37 C (but can grow from 4-42 C) Gram (-) bacillus with outer Part of the normal flora of the GIT: opportunistic 1) Adhesins: colonize GTU or GIT envelope pathogen despite voiding or peistalsis Increased risk of disease with: hospitalization, poor personal hygiene, travel to countries with All other Enterobacteriace features 2) Exotoxins poorly developed sanitary practices, suboptimal immune defences 3) H and K antigens - relative Public hygiene systems in developed nations O antigens used for strain typing, importance/ presence of these factors play a significant role in the relative rarity of E. e.g. O157 : H7 depends on genetics of the strain + site coli infections of infection + condition of host

Hot tub folliculitis

1) Plague vaccine (develop only partial immunity)

2) Quarantine

3) Rodent control

One of the most difficult bacterial infections to treat and control:

1) Many ABC resistance strategies

2) Ubiquitous

3) Most patients with infection are immunocompromised 4) Colonization of surfaces as a biofilm makes them impervious to many ABCs 5) Inappropriate use of ABCs permits their overgrowth and promotes the development of ABC resistant strains

Ecthyma gangernosum

Either:

Prevent by good personal and public hygiene

1) Endogenous infections: in persons with poor personal hygiene and debilitated defences

good BBQ practices are key in the summer

2) Exogenous infections: from contaminated food or water: ABC terapy is not indicated gastroenteritis, neonatal meningitis

Family Enterobacteriaciae

Gram (-) bacillus

Very diverse genus > 2400 distinct serotypes

Facultative anaerobe

Recent DNA evidence suggests only 2 oxidase (-) species:

Salmonella

S. enteritidis epidemiology: Common in the environment Animals are the primary reservoirs for S. enteritides: livestock, fish, poultry/ birds, rodents, humans, reptiles (turtles) Humans most commonly get Salmonellosis from: undercooked poultry, contaminated cutting boards, egg salad, undercooked/ raw eggs

S. typhi

SOD (+)

Disease incidence: peaks in warm summer months. Most common in children and elderly

S. paratyphi and S. enteridis are actually serotypes

Outer membrane: susceptible to drying

S. Typhi epidemiology

1) Surface antigens a) O Ag (on LPS), S. enteritidis gastroenteritis b) V 1 Ag (on capsule) c) species specific fimbria attach to M cells of PP 2) exotoxin (LPS) - responsible for the fevers seen in bacteremic phase of Salmonella induced septicemia enteric fever 3) Invasiveness: penetrate into subepithelial spaces without a toxin Enteric fever mediated process. Rearrange host cell actin (membrane ruffling) 4) Enterotoxins. 3 types: 1&2) LT/ST like toxins (Like E. coli), 3) Cell associated toxin (verotoxin-like)

Improved personal and public hygiene Spread by the 5 "f's": food, fingers, fomites, feces and flies Proper preparation and storate of food: avoid antacids, clean your cutting boards MC'ly symptomatic Tx instead of ABC's S. typhys: oral or parenteral vaccine. 70% effective, transient, frequent side effects.

5) Other: Acid tolerance response gene, catalase, SOD

Humans are the only known animal host Disease in NA primarily associated with foreign travel. Spread by food or water contaminated by infected food handlers Less frequent exposure than S. enteritidis but more likely to get disease because only a small inoculum is needed (S. enteritidis gastroenteritis needs a very high inoculum)

Shigella

Family Enterobacteriacae, Genus Shigella

Gram (-) rod

Humans are the only carriers

Attach and invade M cells in PP

4 species:S. flexneri, S. sonnei, S. boydii, S. dyseteriae

oxidase (-)

Transmission due to fecal-oral route

Use Type II secretion system to cause membrane ruffling (engulf bacteria into host cell)

S. sonnei is the most common cause of shigellosis in the industrialized world

Facultative anaerobe

Very low inoculum (only 10-100 baccili)

Shiga toxin (only S. dysenteria) disrupts protein synthesis

S. flexneri is MC in developing world

Significant outer membrane

Most cases in children 6 months - 10 years

Can proceed to damage glomerular epithelial cells (HUS) in susceptible persons

Does not ferment glucose

Family Vibrioacae, genus Vibrio

Vibrio Cholera

Gram (-) bacillus, comma shaped

Adule infx: contact with children, or male homosexuals Populations at risk: anyone exposed to carrier e.g. daycare centers, nurseries, nursing homes, military barracks, prison, poor sanitation communities Ubiquitous in marine environment - even if 1) Cholera toxin complex A-B toxin: increased salinity and temp 10-30 C. structurally and functionally similar to Contaminated shellfish/seawater is most head-labile enterotoxin A of E. coli common way to transmit disease - B toxin: binding, A toxin: increase Asymptomatic human carriers cAMP, cause electrolyte shift, watery diarrhea

Many species: C. parahemolyticus, V. vulnificus and Vibrio choleara are MC Motile, single polar flagella cause of human disease 200 serotypes: O1 and O139 cause Oxidase (+) Relatively high infective dose classic cholera EI Tor (O1) biotype is MC in world Wide temperature range (18-37) Most cases in NA are from returning travelers today Most need salt for growth (except V. cholera)

Family Bacillaceae, genera bacullus

Gram (+) bacillus. Single or paired "joined bamboo rod"

B. anthracis - anthrax

culture - "medusa head - long, serpentine chains"

B. cereus - gastroenteritis

Colonies - non-hemolytic, sticky

Baccilus anthracis

Gram (+) bacillus

Low mortality compared to B. anthracis

Baccilus cereus

Same as Enterobacteriaceae in general: hygiene, removal and isolation of linens/diapers ABC used to shorten course and control spread but high likelihood of ABC resistance Unlike Salmonella they are resistant to St acid (therefore a much smaller infective dose)

Aggressive fluid/ electrolyte replacement (oral/IV)

Cholera

ABC's reduce exotoxin and more rapidly eliminate organism No long term human carriers (unlike S. typhi) Vaccine: limited usefullness, short lived protection

2) Adhesins 3) Mucinase 4) Siderophores - sequester iron

5) Neruamidase 6) Hemolysin - increase intracellular Ca, therefore inc. chloride secretion Primary reservoirs: domestic herbivores (sheep, Capsule - anti-capsular Abs are NOT goats, cattle, horses) protective Toxin: 3 parts that work together: Three routes of transmission: Inoculation of Protective Ag (binding, anti-phagocytic), skin, inhalation of spores, ingestion of lethal factor, edema factor (stim contaminated food. adenylyl cyclase) Developing countries: endemic, can't affort to vaccinate livestock Developed countries: occupational disease and biological warfare Ubiqutous distribution

Shigellosis

Heat stable enterotoxin - causes emesis. Found in contaminated, improperly refrigerated rice dishes

Cutaneous anthrax

Pennicillin and ciproflaxacin

Inhalation anthrax

Prevention difficult due to long lived spores

Ingestion anthrax

Two types of gastroenteritis:

Heat labile enterotoxin - similar to 1) emetic disease - heat stable enterotoxin of ETEC and Vibro cholera enterotoxin 2) diarrhoeal disease - heat labile - profuse, watery diarrhea enterotoxin Also causes panopthalmitis - contaminated meat, vegetables inflammtion of entire eye posttraumatic injury Cereolysin - involved in eye damage Phospholipase C - involved in eye damage

No person to person transmission with inhalation or ingestion antrax Vaccinations (military), burn/ bury infected animals Gastroenteritis: No ABCs. Rapid consumption of food after heating. Proper refrigeration of uneaten portions. Panopthalmitis - early, aggressive ABCs. Resistance. EMERGENCY!

Necrotic toxin - involved in eye damage Small (0.3-0.6 um) filterable unlike other bactera

#1 bacterial cause of gastroenteritis and bacterial endocarditis in USA (most common is C. jejuni

Adhesins, enterotozxin, cytopathic toxin - not well understood

Gram (-) bacillus - "S or gull-wing shaped"

Zoonoses - poultry, birds, cats/dogs, rabbits, mink, insects, pigs, bulls

Need high infectious dose - reduced with hypochlorhydria, TUMs, milk

Motile - single polar flagella

Transmitted via raw milk and water

Gastroenteritis Guillian Barre syndrome

Campylobacter spp. Microaerophilic (reduced O2, increased CO2) and thermophilic (42 C) Slow grower > 2 days Closely resembles campylobacter

Found in stomach of humans, primates, pigs, cheetas, dogs, cats, ferrets, mice, rats

Surviva acidity: Bacterial acid inhibitory protein. Urease. Heat shock protein. Flagella. Mucinase/ phospholipase

Type B (infective) gastritis

Gram (-) bacillus: gram stain is variable. Sprial shape in fresh culture, coccoid in older culture

Only found in gastric antrum and body

Adhesins

Peptic ulcer disease (PUD)

Clostridium spp.

Only <20% of people, regardless of age whi Resist immune clearance test + for H. pylori also get PUD

very slow (2-6 day) growth in complex media

Form of transmission not clear

temp 30-37 C (not 42 like campylobacter) Gram (+) bacilli MC anaerobic Spore formers

Gram (+) "plump, rectangular" rod

Clostridium perfringens

Microaerophilic - survive relatively anaerobic environment of ST

urease (+)

non-motile but rapid growth on sheeps blood agar Replicated in 10 min!

Gastric adneocarcinoma Gastric mucosa-associated lymphoid type (MALT) B cell lymphomas

Pro-inflammatory: LPS

Triple theory: proton pump inhibitor (omeprozle), clarithromycin, metronidazole, bismuth (dec acid and 2 ABCs) Prevention: stop smothing, drinking, moderate pickled and salt-preserved food consumption Avoid nitrates (smoked and processed meats, nitrosamines (BBQ, charred meats)) Reduce stress Eat healthy stufff. Natural shizzle.

Tissue damaging: PAF (platelet agg factor) hypersecretion of gastric acid

microaerophilic

Family Bacillaceae 3 Classes: Histotoxic: C. perfringen Enterotoxigenic: C. difficile Paralytic: C. tetani, C. botulinum

prevent with proper preparation and storage of food, avoid raw milk, proper water treatment Guillian Barre syndrome: no treatment, proper storage of food

Peak incidence in warm months, young adults (20-29)

Flagellated, highly motile "corkskrew Developing countries high colonization, motion" developed countries low colonization

Helicobacter pylori

Gastroenteritis: short course, selflimiting, no ABC's unless high risk

Ubiquitous: soil, GIT of humans and animals

5 toxin specific types: Type A: Ubiquitous: soil, GIT of humans and animals, permanent soil inhabitant, responsible contaminated water. MC harmless saprophytes. for most human disease (B-E responsible for animal disease) C. perfringens need devitalized tissue to grow Spore formation - long term survival in best environment and throat Toxin formation: alpha toxin - most Disease MC after trauma that causes ischemia: tissue damage. Phospholipase C lowered pO2 and pH favors C. perfringens activity increases vascular permeability growth --> lyse cells beta toxin: necrotizing enteritis, HTN (inc chatecholamines)

Simple wound infection Anaerobic cellulitis C. perfringens myonecrosis C. perfringens food poisoning

proper cleansing of wound, debridement of affected tissue, ABCs, byperbaric O2 chamber

Gram (+) rods

Clostridium difficile

obligate anaerobes, spore-forming

Gram strain variable: (-) in old cultures of fresh wounds, (+) in fresh culture long, thin bacillus with "tennis raquet" morphology

Ubiquitous - spores last for years in soil, sewage, feces contaminated soil

Spores - survive adverse conditions

Present in GIT of cows, horses, some humans

Tetanolysin

difficult to grow: sensitivy to O2 obligate anaerobe. Relatively inactive metabolically (unlike C. perfringens)

Tetanospasmin: heat labile neurotoxin (one of the most potent toxins). Causes Developed world: low incidence due to spasdic paralysis. 2 part toxin: B chain immunization, herd immunity, urbanization. binds R in neuronal membrane. A chain Developing world: higher incidence due to rual, moves to post-synaptic terminals in agricultural societies, low immunization. CNS and irriversibly inhibits the release of GABA and glycine

Gram (+) bacillus, "sausage shaped"

Ubiquitous - soil, sedaments of lakes and ponds, and decaying vegetation

Clostridium tetani

Clostridium botulinum

Toxin A (enterotoxin) - inc cytokines Can be a normal part of GI flora without causing neutrophils. Hemorrhagin necrosis in disease pseudomem. Colitis Toxin B (cytotoxin) - depolymerize MC after broat spectrum ABCs and Proton actin. Marker for more pathogenic pump inhibitors (PPI's) strains. Hyaluronidase - inc spread between tissues Spore formation Adhesion factor - to colonocytes

Strict aerobe

Beta hemolytic on sheeps blood agar

Neisseria spp.

Produces one of the most potent exotoxins known to humans Gram (-) diplococci, "coffee bean" Two main Human pathogens: appearance 1) N. meningitidis - normal colonizer of Transparent, non-pigmented nasopharynx or cause disease colonies on chocolated blood agar Facultative anaerobe 2) N. gonorrhoeae - strict pathogen Can ferment glucose and maltose AKA meningococci (onlke N. gonorrhoeae which only ferments glucose)

Asymptomatically colonize nasopharynx or cause meningitis, meningococcemia or pneumonia Decrease risk of getting disease with breast feeding and healthy immune system

transferred via close contact with respiratory droplets (e.g. daycares, military barracks). Classmates in school not close enough. MC carriers are asymptomatic adults Disease MC in dry, cold months

Termed "the gonococcus"

Humans are sole natural carriers

Need intimate sexual contact. MC in 15-24 year olds. Fastidious growth in culture: NO growth with drying (not on toilet Increased risk if female, multiple sex partners, seat), need humidity and increased blacks, residents of SE USA CO2 Gram (-) diplococci

Neisseria gonorrhoeae

2nd most common STD in the US (chlamydia is #1)

Difficult to tx because spores are resistant Prevent by hygiene and prescribe ABCs with probiotics

Tetanus

Women are MC'ly asymptomatic carriers

Prevention: no natural immunity unlike many other diseases Active immunization - tetanous toxoids: booster every 10 years

Part of DPT vaccine. Proper wound care and umbilical stump care.

Spore formation - one of the mose resistant: hours at 100 C and 10 Food borne botulism "Intoxication" minutes at 120 C. Also -190 C and irradiation Botulinum toxin: one of the most potent neurotoxins. Two parts: B - protects Infant botulism "infectionfrom ST acid. A part - neurotoxin intoxication" specific to irreversible binding to cholinergic neurotoxins Inhibits acetylcholine release at presynaptic terminals and therefore, Wound botulism flaccid paralysis (opposite tetanospasmin) Unclassified botulism

MC cause of baterial meningitis in infants through adolescence and in young adults

Neisseria meningitidis

MC causes post-ABC diarrhea and Discontinue ABCs, maintain pseudomembranous colitis fluid/electrolyte balance.

Support! Adequate ventilation, flush GIT - gastric lavage, IV ABCs, trivalent botulinum antitoxin Prevention - food preparation. Acid pH (canned fruit is OK) - grow best at pH>4.5 (alkaline risky) Refrigerate (Can't survive <4C). Heave for min 20 min at 80 C. Check cans (swollen from gas release) Don't give honey to infants under 1 years old

Colonization of nasopharynx - pili attach Meningiococcemia - mild disease Proper hygiene to con-ciliated columnar cells Host immunity - need specific Ags against capsule and complement sys Bacteria enters host cell and replicates in phagocytic vacuoles - capsule is also anti-phagocytic

Meningiococcemia - marked disease Meningococcal meningitis

Good diet Polysaccharide vaccine - not for children <2. For travelers. Avoid close contact with infected persons

LOS expressed

ABCs

No exotoxin - host damage is from gonococcal induced inflammatory response Anti-phagocytic - negatively charged capsule. Highly variable structure. Pili: tissue trophism: non-ciliated epithelial cells of foreskin, vagina, fallopian tube. LOS - classic endotoxin activity (like LPS). No strain specific O antigens (unlike LPS) Fe 2+ binding proteins IgA protease - destroys IgA Bata lactamas - degrades penicillin

Gonorrhoeae in males

Gonorrhoeae in females

Disseminated gonorrhoeae

Opthalmia neonatorum

Currently no longer use penicillin: resistance (beta-lactamase, need too high dose, change cell surface so ABC can't penetrate cell) Prevention: safe sex!

2 main pathogenic spp:

H. influenzae - encapsulated Heaemophilius spp.

Small, gram (-) coccobacillus (pleomorphic)

Capsule (PRP capsule). Determines Primarily a pediatric problem (<5 yo). Since the serotype and virlence and trophism. vaccine in 1987, now a pediatric problem in the Invasive disease MC HiB. Antideveloping world. phagocytic. Anti-Hib capsule Abs determines severity of disease.

Fastidious growth requirements: X Also increased risk in elderly (esp with COPD, factor (hematin) and V factor (NAD). smokers, alcoholism, altered mental state, Chocolate agar (heated sheeps hospitalized) blood) non-spore formers, non-motile

H. ducreyi - non-encapsulated Non-encapsulated strains: colonize both upper and lower respiratory obligate parasites on mucous tracts (cause sinusitis, OM, bronchitis, membranes of humans and animals pneumonia) Encapsulated strains (serotype b) can become systemic (meningitis, epiglottitis, cellulitis). Vaccine is against this strain only

3 human pathogens:

Gram (-), very small bacili (rodlike)

Most notorious is Bordatella pertussis strict aerobes (whooping cough)

Bordatella Spp.

Family Treponema, order Spirochaetalis

1 species cause human disease (strict M/C strict anaerobes human pathogen): Treponema pallidum Treponema pallidum (2 subspecies)

Treponema pertue

Pili - damage respiratory ciliated epithelium

H. Ducreyi: Treatment with ABCs. Safe sex!

LPS - responsible for mengitis

Can only cause disease in humans reportable disease

Pertussis toxin - increase Adenylate cyclase. cAMP respiratory secretions/ mucous. Binds ciliated epithelium and kills NK cells, monocytes, macrophages, neutrophils

> 1 million deaths per year. Most common in developing countries in children < 1 year old. Spread by infectious droplets.

Adenylate cyclase toxin (cyclosin) increase cAMP

Tracheal cytotoxin - part of the PG layer. Cause ciliostasis and then damage to ciliated epithelial cells cough - IL-1 = fever Dermonecrotic toxin - heat labile, Fastidious growth - humiditiy, No long term imminity - can get disease more vasoconstriction of peripheral blood specialized media. (Charcoal, blood, than once vessels, hemorrhage, localized NAD-enriched) ischemia Filamentous haemagglutin and other adhesins: attachment to ciliated "protection" in developed countries due to DPT epithelial cells and PMNs. Intracellular vaccine survival protects against clearance by humoral immunity LPS - two types, lipid A and lipid X Small, thin, coiled spirochetes Humans are the only reservoir of disease: Outer Membrane - proteins adhere to can't visualize via Gram stain and increased risk if 20-35, urban areas, drug user, host cell. High lipid to escape cell light microscopy prostitution, lo SES immunity. oxidase (+)

Conjugated HiB vaccine (purified PRP). 2 types.

Whooping cough

ABCs are of limited use (disease is not recognized until peak of infectiousness has passed)

Increased incidence in older individuals waning immunity

3rd most common STD in the USA

Fastidious growth - only in cultured very labile, susceptible to drying - only spread rabbit epithelial cells, doubling time with direct contact of warm, moist infectious 30 hours lesions

Mostly supportive (hydration, control secretions, maintenance of airway)

Erythromycin is ABC of choice

Prevention - DPT vaccine. 2, 4, 6, 15 months and 4-6 years. Used to use whole cell vaccine (DTwP) but now use acellular B. pertussis (DTaP) - "fever side effects"

Syphilis = pig lover!!

Hyaluronidase - spreads through tissue LPS - similar to gram (-) LPS

High dose penicillin - maintain in blood for a few days since it divides every 33 hours Prevention: hygiene (spirochetes destroyed by soap and water, temp >42 and drying) Safe sex practices

Contagious only during primary stage and rash Motile - "corkskrew motility" via thin of secondary stage - not highly contagious (only fibrils at both ends 30% chance after single sexual contact) Active genital lesions increase risk of HIV infection

2 separate genera: 1) Chlamydia: Chlamidia trachomatis

VERY small Gram (-) bacillus with:

2) Chlamydophila: C. psittaci (from birds), C. pneumonia

Virus-like properties - filterable and gains access through minute abrasions or obligate intracelular parasites lacerations

Only affects humans

Bacteria-like properties - inner/ outer Limited tissue trophism membranes, bacterial ribosomes, contain DNA, RNA and LPS

Chlamydia

Strains causing LGV (lymphoma granuloma Unlike other bacteria there is no venereum) can cause systemic infections by PG layer, therefore no Gram stain entering lymphatic system Unique growth cell cycle within host clinical signs and symptoms due to direct cell - EBs (elementary body) and destruction of cells during replication and host RBs (reticylite body) inflammatory response No long term immunity - re-infection leads to vigorous inflammatory response Leading cause of preventable blindness in developing countries most commonly in children due to poor hygiene Spread by droplets, hands, contaminated clothing, eye make-up, flies Can get from toilet seat - EB is resistant to the environment!

EB: major outer membrane proteins tightly cross-linked: extracellular survival and initiation of infection Reticulate body: Less cross linking so more fragile, adapted for intracellular growth; metabolically active Inclusion body: Phagosome with accumulated RBs: high amount of glycogen, therefore stain with iodine

Trachoma disease

Treatment MC also have presumptive TX for gonorrhea

Trachoma inclusion conjunctivitis

Prevetion: hygiene: hand/face washing

Chlamydia urogenital infections

Practice safe sex

Reactive arthritis (Reiter's syndrome) Lymphogranuloma vererum Chlamydiophilia pneumonia Chlamydophila psittace

>70 spp, many associated with disease in humans M. tuberculosis - TB Mycobacterium

M. bovis M. leprae - leprosy

Runyon classification depending on growth characteristics and pigments produced with light Acid fast (fungus like), weakly Gram (+) bacillus obligate aerobe fastidious, slow growth - one of the slowest dividing microorganisms (need ABCs for long time)

M. avium Complex - assoc with AIDS M. Gordonae (won't talk about) Cause of more fatalities worldwide than any Contains much mycolic acid in its cell other infectious disease (humans are the only wall - acid fast, resist drying, known carrier) detergents, acids/bases

Mycobacterium tuberculosis

Similar to M. tuberculosis but:

Mycobacterium leprae

MC'ly person-person transmission via infectious Protein polypeptides on cell surface aerosolized particles - very small inoculum immongenic, source of PPD for needed Mantoux test Inhaled to terminal airways --> resist Increased risk if immunocompromised, killing by phagosome/lysosome fusion homeless, substance abuse, elderly, chemo, and evade humoral immunity b/c of tavelers, first nation persons intracellular growth Spread to LN and into bloodstream to other tissues No known toxin: tissue destruction is due primarily to host immune response form tubercles - develop into caseous granulomas Ghon complex - initial lung lesion and locally enlarged LNs Rare in US, common in India, Brazel, Myanmar, Indonesia, Bangladesh. MC in men and Capsule children.

Can not be articicially cultured (need Armadillos are naturally infected and provide live mice or armadillos) reservoir

Preference for lower temperatures limits infection to skin and nasopharynx

Grow in globi bundles (encapsulated Spread via respiratory route or contact with globs of rods in tissues) break in skin

Intracellular survival - in Histiocytes and Schwann cells

Treatment: "Denver protocol" multi-drug cocktail for >3-6 months. Quarantine. Problem: MDR-TB

TB

Prevention: Diet/ robust immune system BCG vaccine - not as effective in adults, not used in immunocompromised, give false (+) later on

Tuberculoid (paudibacillary)

Emptional support

Lepromatous (Multibacillary)

ABC for years Surgery and grafts, physical therapy Hot wax baths

Similar to M. tuberculosis but only case opportunistic infections Mycobacterium avium intracellulare complex

MC'ly disease in HIV/ AIDS patients but can cause disease in birds and pigs Also can cause lymphadenitis in children

Ubiquitous in water and soil

MAC disease

ABCs

Many different spp

Gram (-) spirochete, spiral shaped

Borrelia burgoderferi

Larger than other spirochetes and more complex nutrition required Microaerophilic Internal flagella

Borrelia spp.

Contain cholesterol in cell wall (unlike other bacteria)

Leptospira spp

Dormant in glial cells

Spirochetes release neurotoxins that MC vector borne disease in USA (no person to affect pre and post-synaptic person spread) membranes vector: deer tick (Ioxdes scapularis/ Ioxdes Autoimmunity?? pacificus) Reservoir: white footed mouse or white tailed deer MC in Northern temperate zone esp New York Sate Increased risk in grassy, wooded areas and mid May-mid August One of the fastest growing infectious diseases in the world Can mimic signs and symptoms of MANY diseases! Zoonotic - rodent (rat) and domestic animal (dog) reservoirs

Spirochetes enters via contaminated urine: entry to broken skin and mucosa

L. biflexa - free living, non pathogenic obligate aerobe

Humans are accidental hosts: MC'ly acquire disease via contact with infected urine

Unknown mechanism of tissue damage

L. interrogenes - human pathogen leptospirosis

Replicate in endothelium lining of Increased risk in tropical areas and in men capillaries (affect meninges, LV, KI) and (farmers, veterinarians, back-packers, hunters) interfere with blood flow

2 main:

Gram (-), very thin, tightly coiled spirochete

Cause relapsing fever and Lyme disease (Boreellia burgodorferi). Need ticks as vestors

minimal nutrition requirements: LCFA, vitamin B1 and B12

Lyme disease

Avoid potential tick infested areas

Neruoborelliosis

Light colored clothing, tuck pants into socks and shirts into pants Insect repellants Check and remove ticks Treatment: ABCs, vaccine not very effective

Leptospirosis

Survive moist, slightly alkaline environment for many days (up to 6 weeks in urine soaked soil). Susceptible to drying, detergents, heat (50 C), salt water Internal periplasmic flagella (like other spirochetes) Many spp

Originally thought to be viruses

Human pathogen is Rickettsia ricketsii (cause Rocky Mountain Spotted Small bacteria Fever) Rickettsia spp.

Need arthropod vectors - hard ticks (dog tick or Must be exposed to tick >24 hours wood tick) - Dermacentor Inc when outdoors, miliatry activity in endemic areas

Structurally similar to Gram (-) bacteria (min PG layer, LPS, MC in children and in summer months sysceptible to ABCs, need O2, have metabolic enzymes) No flagella, weakly adherent slime capsule

Worst prognosis if elderly, males, G6PD deficiency

Rocky Mountain Spotted Fever

Treatment: aggressive ABCs

Multiply in skin site first, then affect other organs

Control: same as other tick borne diseases

Weak endotoxin, host immunity plays no role in pathology - survive within phagocytes, tissue damage due to multiplication in vascular epithelium and causing leakage - leads to dec perfusion and organ failure

Almost impossible to get rid of ticks (can survive up to 4 years without feeding)

Microbe 1

Yersinia enterolytica

System

Condition

Signs and Symptoms

GI

Yersinia entrolytica gastroenteritis/ Yersinosis

Need a large infective dose, ingest contaminated food product. 4-6 day incubation. Right sided abdominal pain. Lasts for 1-2 weeks. Can progress to perforation of ilum and skin rash (erythema nodosum). Can get mesenteric adenitis in children (mimics acute signs of appendicitis)

2

Yersinia pestis

Circulatory

Bubonic plague

3

Yersinia pestis

Respiratory

Pneumonic plauge

4

Yersinia pestis

CNS

Septicemic plague

5

Pseudomonas

Circulatory

Endocarditis

6

Pseudomonas

CNS

CNS infections

7

Pseudomonas

Skeletal

Bone and joint infections

8

Pseudomonas

Eye

Bacterial Keratitis

9

Pseudomonas

Urinary

UTI's

10

Pseudomonas

GI

GIT infections

11

Pseudomonas

Ear

Swimmer's Ear

12

Pseudomonas

Systemic

Bactermia

13

Pseudomonas

Skin

Hot tub folliculitis

14

Pseudomonas

Skin

Ecthyma gangernosum

15

Escherichia coli

CNS

Neonatal Meningitis

16

Escherichia coli

Systemic

Septicemia

17

Escherichia coli

Urinary

UTI's

18

Escherichia coli

GI

Gastroenteritis - Enterotoxigenic (ETEC/ VTEC)

Nausea/ Vomiting

Get bitten by infected flea, 2-6 days later get high fever, chills. Not large but painful buboes in groin, axilla, neck. Prostration with rapid, thready pulse, delerium. Bubonic purperea: vasculitis of superficial blood vessels cause bleeding into skin - black death. Can spread to blood then to lungs. Fatal within days (75% mortality) Hematogenous spread from infected buboes or aerosols from infected person. Only 2-3 day incubation. Fever, malaise, hemoptysis, dyspnea. Highly virulent, rapidly fatal form of bronchopneumonia (90% mortality) Direct deposit of bacteria into open wound or orifice. Most common in children. Rapidly fatal meningitis before buboes form. Especially tricuspid valve. Increased risk with IV drug users and prosthetic HT valves meningitis, brain abscesses Especially fibrocartilaginous joints of axial skeleton. Most comon pathogen in osteochondritis after puncture wound to the foot.

Fever

Diarrhea

Yes

Watery or bloody

DDX and Lab Dx

Black plague 2 types: Urban: affects humans and can cause 3 types of plague. Rats are the main reservoir, rat flea (Xeopsylla cheopsis) is main vector. 2) Sylvatic (Woodland): disease of wild rodents found everywhere but Australia

High

Yes

Most common cause of bacterial keratitis and neonatal opthalmia. Increased risk iff immunocompromised, contaminated eye drops (contacts), hypoxic damage from prolonged contact wearing, corneal trauma, eye operations. Can lead to blindness. Most common bacteria is S. aureus unless contact wearer, then P. aeruginosa.

Unilateral, acutely painful, photophobic, intensely injected eye. Decreased visual acuity. Profuse tearing, thick ropey mucopurulent discharge. Edematous cornea and eyelid

3rd leading cause of nosocomial UTIs. Prolonged indwelling catheters. Any part of the tract. Eg. Perirectal, pediatric diarrhea, gasteroenteritis, necrotizing enteritis Can get chronic supporitive OM, malignant otitis externa or Swimmer's ear (acute diffuse otitis externa). Weber test: laterlize to affected side. Rinne test: AC>BC.

Initial pruritis and fullness in ear. Increased pain/tenderness on palpation. Otorrhea (?), Possible hearing loss (mild erythema and edema of external auditory canal. Dull injected TM with displaced COL). No systemic signs. Primarily nosocomial. Increased risk if immunocompromised. Similar clinical presentation as other bacteremias but with higher mortality. After breakdown in skin integrity (burns, trauma, cuts, dermatitis). High moisture conditions or immunocompromised. Pathognomic Pseudomonas skin infection. Erythematous vessels become hemorrhagic, necrotic and ulcerated with a fruity odor. Can have rapid necrosis to adjacent tissue (potentially fatal)

Most commonly caused by E. coli and group B strep. Most isolated strains from babies have K1 capsular Ags (maternal anti-K1 Abs are protective).

Colonization of infants with E. coli is common but rarely leads to disease

E. coli is most common cause of enterobacterial septicemia (45%), then K. pnemonia Very common infection: 10-20% of all women will have at least 1 in their lifetime. Spread is from GTU: ascending infection. Virulence factors: special adhesins are used to attach to uroepithelium and resist flushing durin micturation (decrease attachment with D-mannose, blueberry & cranberry juice). Lab dx: pyuria, hematuria, bacteriuria.

Usually results from spread from GIT or GTU. Increased mortality if immunocompromised or due to complication of intestinal perforation.

Cystitis: dysuria, urgency, increased frequency, incomplete voiding. Pyelonephritis: same as cystitis but more severe and with fever, loin pain and (+) KI punch.

Most important cause of traveler's diarrhea and infant diarrhea (in developing Cramps, nausea, countries). Symptoms take 3-4 days to resolve. Symptoms similar to cholera vomiting (rare) but much milder.

Low grade

Watery

Gastroenteritis (6 types) - most common E coli infection in normally healthy persons. Exotoxins: St a/ST b: heat stable, stimulate guanylyl cyclase. LT1/ LT 11: heat labile, stimulate adenylyl cyclase. Induce fluid and electrolyte loss: watery diarrhea

Variable onset (1-4 days). Intense abdominal cramps. Can progress to colonic ulceration and more severe sequelae. Similar disease to Shigella

19

Escherichia coli

GI

Enteroinvasive (EIEC)

20

Escherichia coli

GI

Enteropathogenic (EPEC)

Yes

Yes

21

Escherichia coli

GI

Enteroaggregative (EAggEC)

Yes

Low grade

22

Escherichia coli

GI

Enterohemorrhagic (EHEC)

Yes

No fever or just low grade

23

Escherichia coli

GI

Diffuseaffregative (DAEC)

24

Escherichia coli

Urinary

HUS

25

Salmonella enteritidis

GI

S. enteritidis gastroenteritis

26

Salmonella typhi / Salmonella paratyphi

Systemic

Salmonella induced septicemia

3-4 day incubation. Severe abdominal pain. Most commonly self-limiting in 410 days but can progress to HUS (hemolytic uremic syndrome). Spread via: undercooked beef or other meat, feces contaminated water, unpasteurized milk, fruit juices, raw veggies/fruit.

Abdominal pain. Irritability, lethargy or seizures. HTN, pallor. Anuria or oliguria. Acute renal failure - destruction of renal glomeruli. Potentially fatal sequelae of gastroenteritis in 10% of children. Spread: person to person. Handwashing is important and child must be isolated until 2 consecutive (-) stool cultures. Occurs 6-48 hours after ingestion of contaminated food or water. Abdominal cramps, h/a, myalgia. Most commonly self limiting (2 days to 1 week). Low mortality but increased risk with elderly and children.

Enteric fever

Non-specific systemic symptoms (H/A, malaise, myalgias, and anorexia). Rose coloured spots on abdomen (erythematous, maculopapular, blances with pressure, only 50% of patients). Complications: GI lesions, Toxemia, meningitis, osteomyelitis, endocarditis. 1-3% become chronic carries.

28

Shigella

GI

Shigellosis

GI symptoms are caused by Shiga toxin. Enterotoxic, neurotoxic and cytotoxic. 1-3 day incumation. Fever and diarrhea proceeds to tenesmus, abdundant blood and pus in stool.

Cholera

30

Bacillus anthracis

Skin

Cutaneous anthrax

31

Bacillus anthracis

Systemic

Inhalation anthrax

32

Bacillus anthracis

GI

Ingestion anthrax

Yes

Most common cause of acute renal failure in children. Lab dx: stool culture (+) for E coli O157 : H7, hemolytic anemia, thrombocytopenia

Non-bloody diarrhea

Most common type of Salmonellosis

MC spread is by food handlers infected with S. typhi (typhoid fever) or S. paratyphi (paratyphoid fever). Bacteria pass directly through intestinal walls. Enter thoracic duct and then blood stream to replicated in Sp, LV, bone marrow and GB. Back into the intestine to cause increased inflammation. This is NOT typhus.

Systemic

GI

Yes

Bloody diarrhea

Most commonly due to S. typhi and S. paratyphi but also seen with S. enteritidis. Increased risk with AIDS, geriatrics and pediatrics.

Salmonella typhi / Salmonella paratyphi

Vibrio cholera

Vomiting

Symptomology similar to other Gram (-) septicemia: 10% of patients develop arthritis, osteomyelitis, and endocarditis

27

29

Yes

Initial watery diarrhea progressing to Bacteria invade and destroy tissue. scant, bloody stool that is leukocyte (+) Bacteria adhere to plasma membrane of mucosal epithelial cells and destroy Non-bloody stool adjacent microvilli. Common cause of infant diarrhea. Cause persistant diarrhea in Persistent, watery developing countries. Subset of EPEC diarrhea that can form aggregates on surfaces (dehydration risk) that they colonize. Most common strain causing disease Initial non-bloody in developed nations. Cause of diarrhea "Hamburger disease" and HUS progresses to (Walkerton). Virulence factor: bloody diarrhea hemolysin. Very low inoculation is needed (100 bacilli) Wattery diarrhea Bacteria are embedded in cell (infants 1-5) membrane of elongated microvilli.

2-3 day incubation. Abrupt onset of watery diarrhea and vomiting. Rice water stools. Severe fluid and electrolyte loss.Hypovolemic shock leads to cardiac arrhythmia, renal failure, muscle cramps. 60% mortality iff untreated, self limiting within a week. No abdominal cramps or fever. Painless papule. Ulcer surrounded by vesicles - necrotic eschar gelatinous edema. MC arms, hands, face, neck. Potentially fatal - 20% mortality (could spread to blood/lymph) . Internal hemorrhage, myalgia, fever, H/A, n/v. Carried by alveolar macrophages to mediastinal LN - prolonged latency. Initial disease: fever/chills, dyspnea, cough, H/A, vomiting, chest/ab pain. Second stage: rapidly worsening fever, pulmonary edema, massive enlargement of mediastinal LNs, shick/death within 3 days. Hemorrhagic meningitis Sx's MC than pulmonary Sx's. IFF upper GI: ulcers, edema, sepsis, regional lymphadenopathy - dysphagia. IFF lower GI: n/v, malaise, systemic s's and sx's, bloody diarrhea

Increasing, remittent

None

Yes

Yes

None

Profuse watery

Bacteremia rare. Infection self-limited. 5% can asymptomatically carry.

Cam resemble ETEC induced gastroenteritis. Lab Dx: rarely seen in Fram stained stool or wound Watery, rice water specimens. Dark field/ phase contrast microscopy: characteristing darting motility. Direct contact with spore contaminated animals/producers. Look at px history: wool worker? Gm (+) bacillus in lesions, no neutrophils. No person to person disease transmission. 87% mortality.

Extremely rare. 100% mortality.

33

Bacillus cereus

GI

Emetic disease

34

Bacillus cereus

GI

Diarrheal disease

35

Bacillus cereus

Eye

Bacillus cereus panopthalmitis

36

Campylobacter jejuni

GI

Gastroenteritis

37

Campylobacter jejuni

Neural

Guillian Barre syndrome

38

Helicobacter pylori

GI

Type B (infective) gastritis

39

Helicobacter pylori

GI

Peptic ulcer disease (PUD)

40

Helicobacter pylori

GI

41

Helicobacter pylori

Systemic

42

Clostridium perfringens

Skin

Simple wound infection

43

Clostridium perfringens

Skin

Anaerobic cellulitis

44

Clostridium perfringens

Skin

C. perfringens myonecrosis

45

Clostridium perfringens

GI

C. perfringens food poisoning

46

47

Clostridium difficile

Clostridium tetani

GI

Musculoskeletal

Gastric adneocarcinoma

Contaminated rice, not refrigerated. 15 min-4hr incubation. Self limiting >24 hrs. Contaminated meat, veggies, sauces. 8-12 hr incubation in GIT. Self limiting <24 hrs

Yes

No

No

Nausea

No

Bloody diarrhea

Post-traumatic, penetrating eye injury or hematogenous spread. Pain, H/A, drowziness, swelling. Muddy grey iris, turbid aqueos humor, precipitate on posterior surface of cornea. Rapid <48 progressive loss of light perception

Yes

2-11 day incubation. Foul smelling, watery diarrhea progressing to profuse bloody diarrhea. Resolution in 3 days - 3 weeks. Residual histological damage to mucosa of jejuni, ileum and colon.

Yes

Watery --> bloody

Idiopathic, peripheral polyneuritis 1-3 weeks after mild above conidition. Progressive, symmetric pain and weakness in extremities - might ascend to trunk, face, thorax. Self limiting (few weeks to months) with complete recovery.

Many causes. Also immunizations, pregnancy, URI, EBV, CMV, Hodgkin's lymphoma. Autoimmune link: cross reactivity with glycosphingolipids on surface of neural tissue

Epigastric pain, abdominal tenderness, bloating, nausea, anorxia, dyspepsia. Epigastric tenderness on percussion, foul smelling breath, hematemesis (coffee grounds)

30-50% of people with gastritis have H. pylori but most commonly asymptomatic. Lab Dx: 13C urea breath test, anti-H. pylori Abs (IgG), gastroscopy with biopsy, CLO test (+(

Expecially dodenal ulcers. Burning, gnawing upper GI pain 1-3 hours after meals. < night, > eating or > antacids. Anemia, epigastric tenderness. Sequelae of untreated chronic gastritis. Classifies as a class I carcinogen. Fatigue, weight loss, low grade fever, night pain. Epigastric/abdominal mass. Hemoccult (+) stools, anemia.

Nausea

Endoscopy, urea breath test, serology (anti-H. pylori Abs) Nausea, sometimes vomiting

Low grade Chronic H. pylori infection assoc with B-cell lymphoma. No evidence that eradicating H. pylori prevents the progression of gastritis to carcinomas

Gastric mucosa-associated lymphoid Dysphagia, dyspepsia, weight loss, GI bleeding - hematemesis. type (MALT) B cell lymphomas

Pseydomembranous colitis

Tetanus

MC, no clinical consequences Trauma and favourable conditions. Organism spread through subQ tissue spares fascia and deep muscles. Pain, redness, inflammation, superficial skin discoloration and skin necrosis. Gas forms develop suppurative myostitis foul smelling discharge. No muscle necrosis, no systemic signs and symptoms. Rapid worsening of cellulitis. Trauma and 1 week incubation. Rapid onset of intense pain, extensive muscle necrosis (blue black, edematous, does not bleed or contract on stimulation), toxic delerium. Progress to shock, renal failur, death within 48hrs if untreated. Much damage due to alpha toxin and gas bubbles. MC in areas of poor blood supply. Need to perform debridement and examine inderlying tissue. Ingest meat (refrigerating and re-heating destroys enterotoxins) Large infective dose. Short incubation: 8-24 hrs. Abdominal cramps. Self limiting > 24 hrs.

Range from mild diarrhea to colitis to potentially life-threatining pseudomembranous colitis.

MC form of tetanus. Bacterium introduced by trauma to skin: rusty nail, animal bites. 3 Early signs: 3 day-2 week incubation. Muscle stiffness/ ridigity, exaggerated DTRs (deep tendon reflexes). Trismus (lockjaw), risus sardonius (rye smile), drooling, dysphagia, diaphoresis, irritabiliey. Later signs: opisthotonus (backward arching), flexion of arms, extension of lower extremitis. Complications: HTN/hypotension, tachycardia, pneumonia, dehydration, bone fractures, meningitis, Rh incompatibility. Other forms: 1) localized (to point of infection, less common than generalized), 2) Cephalic (rare but poor prognosis, from improperly cleaned umbilical stump), 3) Neonatal - first sign, difficulty sucking 8-10 days after birth.

Fast growth of culture on sheep's blood agar. Nagler's reaction on egg yolk agar. Gram (+) rods in tissue specimens with no leukocytes.

None

None

Watery

Prolonged (dehydration)

Pseudomem colitis confirmed by biopsy - multiple, raised white/yellow exudative plaques adhering to colonic mucosa. In vitro cytotoxicity assay in culture cells. Immunoassay for C. difficile toxins A and B. Sigmoidoscopy. Fecal leukocytes. Patient history. Clinical S's and Sx's. Gram stain culture not that important diagnostically - only 30% of people with tetanus are culture (+). Treatment: tetanospasmin binds irreversible and therefore, can only treat symptoms until nerve terminals regenerate. Either penicillin high doses or tetracycline, or passive immunization - bind free tetanospasmin and decrease progression of disease.

48

Clostridium botulism

Musculoskeletal

49

Clostridium botulism

Musculoskeletal

50

Clostridium botulism

Musculoskeletal

51

Clostridium botulism

Musculoskeletal

52

Neisseria meningitis

53

Neisseria meningitis

Systemic

54

Neisseria meningitis

Systemic

55

Neisseria gonorrhoeae

Reproductive

Food borne botulism "Intoxication"

Consumption of honey contaminated with spores. MC form of Botulism in the USA. MC in 1-6 months because infant GIT doesn't have as many competitive bowel microbes. Can resemble SIDS iff rapid onset. Non-specific Infant botulism "infection-intoxication" signs: constipation, weak cry, failure to thrive, weak sucking. Floppy baby: acude flaccid paralysis (head, fact, throat), descent to extremities/trunk. Death reom respiratory paralysis (low 1-2% mortality) Very rare, little evidence of clinical infection. Limited paralysis. Same sx's of Wound botulism food borne botulism but long incubation (1-4 days) and no abdominal pain or constipation People over 1 year who have had symptoms of botulism but no documented Unclassified botulism vehicle of transmission. DDX is important. Meningiococcemia - mild disease Persistent (few days to weeks). Arthritis. Petechial skin rashes. Pharyngitis. URI infection 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). Iff untreated can progress to DIC or hammorhage into Meningiococcemia - marked disease adrenal glands (Waterhous-Friderichsen syndrome). Sequelae: none or large areas of necrosis. Deafness. Mortality 100% if untreated, 25% if treated. Occurs with or without meningitis N. mengintidis is 2nd MC cause of adult bacterial meningitis. Triad: fever, Meningococcal meningitis nuchal rigidity, blinding HA. Neurological sequelae (hearing deficits, arthritis, memory loss) low compared to H. influenzae or S. pneumonia

Gonorrhoeae in males

56

Neisseria gonorrhoeae

Reproductive

Gonorrhoeae in females

57

Neisseria gonorrhoeae

Reproductive

Disseminated gonorrhoeae

58

Neisseria gonorrhoeae

Eye

Opthalmia neonatorum

59

Haemophilius influenzae

Systemic

Menigitis

60

Haemophilius influenzae

Respiratory

Epiglottitis

61 62 63

Haemophilius influenzae Haemophilius influenzae Haemophilius influenzae

Skin Skeletal Respiratory

Cellulitis Arthritis Otitis media / Sinusitis

64

Haemophilius influenzae

Respiratory

Pneumonia

65

Haemophilus ducreyi

Reproductive

Chancroid

66

67

Bordatella pertussis

Treponema pallidum

Respiratory

Reproductive

Inadequate sterilization of food: home canned foods, preserved fish. 2h-72 hour incubation. No GI distress - unlike other food poisonings, Dilated, fixed pupils; dry/ "furry" tongue. Bilateral descending weakness - of neck, face, throat. Respiratory paralysis (mortality 32-40%.) No permanent immunity - can get repeated occurances. MC complete recovery in months to years.

No fever - clear sensorium

Low grade

Rapid onset

In children

Fever

95% of men get acute symptoms. MC'ly gonococcal urethritis. Infection usually restricted to mucous of penis. 2-7 day incubation - purulent urethral discharge, red/ edematous urethral meatus, itching, burning, dysuria, urgency. Can progress to peri-urethral abcesses, prostatitis, epididymitis. >50% of women are asymptomatic or mild symtoms. Infection site MC'ly cervix (cervicitis). 2-7 day incubation. Vaginal discharge or abnormal vaginal bleeding, dysuria, urgency, swollen painful abdomen (RUQ). If untreated an ascending infection can develop. Major cause of infertility iff chronic. Secondary: Fitz Hughe Curtis syndrome: periphepatitis (affects liver symptomatic gonorrhea) Rare but MC in women (1-3%). Systemic symptoms or complex syndrome with fever, migratory arthralgias, tender papillary lesions/ rash on extremities. Arthritis: MC'ly mono-articular - knee in females. N. gonorrhoeae is the #1 cause of purulent arthritis in young adults MC'ly caused by N. gonorrhoeae or C. trachomatis. 2-5 days after vaginal birth. Purulent conjunctivitis in newborns infected during vaginal delivery. Sticky discharge, edema/ inflammation. Can lead to scarring and blindness. Reason why newborns get eye drops of 1% sulver nitrate. Same signs and symptoms as other bacterial meningitis - but more insidious onset and increased risk of neurological sequelae. Used to be MC pediatric meningitis, before Hib vaccine Medical emergency, MC'ly in boys 2-4 yo. Dysphagia, drooling, muffled voice, minimal cough. Severe dyspnea. Reddish/ blue patch on cheek or peri-orbital Monoarticular. Large joint. Three MC causes: H. influenzae, S. pneumonia, Moraxella catarrhalis. Might be secondary to influenzae virus damage to respiratory epithelium. Secondary bacterial infection is more life-threatening than primary. STD, most common to developing world. Unlike primary syphilis which causes hard chancre. Sof, purulent, painful ulcer (genitalia). MC males, uncircumcised, tropical & sub-tropical (female MC asymptomatic). 5-7 day incubation. Progress to painful buboes, phimosis, urethral stricture.

Clinical signs and symptoms paramount. Patient history. Culture stool/food for toxin (only > 60% specificy).

Clinical signs and symptoms and CSF analysis. High number of Gram (-) diplococci in PMNs. Clinical signs similar to Chlamydia. Gram stain: sensitive and specific iff men with purulent urethritis. Oxidase (+), Gram (-) diplococci on chocolate blood agar. Genetic probes: PCR.

Fever

Gram stain of CSF. Chocolate agar culture. Agglutination reaction to PRP capsule in CSF and urine.

In children

High

"Thumb sign" on lateral X-ray of neck

Yes

Gram stain of blood Gram stain of blood Gram stain of blood

Unexplained

Gram stain of blood

Whooping cough

Incubation: 7-10 days, sub-clinical. Catarral phase: 2 weeks, looks like common cold: rhinorrhea, sneezing, low grade fever, anorexia, malaise (most infectious stage). Paroxymal stage: 1-2 weeks, dry non-productive repetitive "whooping" cough. Cough ends in vomiting and exhaustion. Convalescent stage: 2-4 weeks. Cough resolves, secondary complications: aspiration pneumonia, seizures, encephalopathy.

Bacteria are best isolated using nasopharyngeal aspirates during catarrhal stage. Culture: difficult humitidy, 35 C, 7 days, specialized agar (only 50% of infected people are culture (+). Throat swabs not as good - need synthetic fiber swabs. PCR. Lymphocytosis (not specific)

Syphilis

Primary: small papule - painless, hard chancre. Painless, regional lymphadenopathy (buboes). Very infectious. Heals spontaneously within 2 months without scarring. Secondary: flu-like syndrome. Painless, localized lumphadenopathy. Diffuse, non-pruritic maculpapular rash, includes soles, palms. Very infecious (kissing). Tertiary (Lues/Leutic): after 3-40 years of latent syphilis. Gummas (flat rubbery tumors anywhere in body - ulcerate and heal by scarring). Affect many organ systems: neurosyphilis, cardiosyphilis. Painless or deep burrowing pain. Congenital: infected mother infects fetus. 1) Intra-uterine death; 2) Congenital abnormalities 3) Born appearing well then several weeks or up to 2 years later: snuffles, widespread desquamating maculopapular rash. (Risk if mother is in primary or secondary syphilis)

Microscopy: no Gram stain, use silver stain and fluorescent stains. Nonspecific tests: VDRL (veneral disease research lab) and RPR (rapid plasma reagin) (+4-6 weeks after infection indicates current active disease but false positive). Specific tests: FTAAbs (fluroscent treponema Ab) and MHA-TP (micro haemoglotunin for Treponema) - indicate past infection

68

Chlamydia trachomatis

Eye

Trachoma disease

69

Chlamydia trachomatis

Eye

Trachoma inclusion conjunctivitis

70

Chlamydia trachomatis

Reproductive

Chlamydia urogenital infections

71

Chlamydia trachomatis

Reproductive

Reactive arthritis (Reiter's syndrome)

72

Chlamydia trachomatis

Reproductive

Lymphogranuloma vererum

73

Chlamydophila

Respiratory

Chlamydiophilia pneumonia

74

Chlamydophila

Respiratory

Chlamydophila psittace

75

Mycobacterium tuberculosis

Respiratory

TB

76

Mycobacterium leprae

Skin

Tuberculoid (paudibacillary)

77

Mycobacterium leprae

Skin / Neural

Lepromatous (Multibacillary)

78

Mycobacterium avium intracellulare complex

Respiratory

MAC diseases

79

Borrelia burgdorferi

Skin / Neural

Lyme disease

Must have spscific attachment to conjuctiva - resist flushing from tears. Begins as conjunctivits. Entropian - eyelashes chronically irritate cornea causing ulceration Adult. Most common 18-30. Genital infection 1st then unilateral mucopurulent discharge in eye. Neonatal: infected mother and vaginal birth. Bilateral, intense papillary conjunctivitis with lid swelling, chemosis, and mucopurulent discharge Women: termed Chlamydia (the drip?) Most commonly asymptomatic (80%) but risk of intertility, miscarriage, ectopic pregnancy. Can cause urethritis, conjunctivits, perihepatitis (pain in RUQ). Pain/ cramping in lower abdomen, dyspaerunia, bleeding between menses. Men: NGU (non gonoccocal urethritis). MC symptomatic (75%) - yellow clear discharge, pain/ tenderness of genitals. Ractive arthritis (Reiter's syndrome) - can't see, can't pee, can't dance with me! Seronegative (Rh-) spondyloarthropathy. MC in young men (20-40 years) that are HLA-B27 positiv. C. trachomatis is MC bacterial pathogen. Unexplained diarrhea, low grade fever. 2-4 weeks later conjunctivits, superficial lesions on palms/ sole/ oral mucosa, asymptomatic polyarthritis, urethritis

Currently MC bacterial STD in USA.

Low grade

TWAR isovar. Human pathogen that can cause atypical pneumonia (mild, persistent cough/ malaise that might progress to lobar pneumonia). Potential link to atherosclerosis, CAD, MS, asthma, Alzheimer's disease? MC in adults. Spread via respiratory droplets. Cause psittacosis. Biggest risk from psittacine birds (parrots, mascaws, parakeets, cockatiels) Transmitted via inhaled dried bird excrement, urine and respiratory secretions. Non-productive cough., rales, mucous plug can block bronchi. Commonly progesses to CNS(encephalitis, convulsions, coma, death)

3-6 year incubation. Strong cellular response, weat humoral. Not infectious. <5 cutaneous macular lesions with hypopigmented centers. Some nerve enlargement and damage. 3-10 year infection. Weak cellular response, strong humoral. Relatively highly infectious. Most destructive - disfiguring skin/bone, cartilage lesions ("leonine face") Diffuse nerve involvement. Erythema nodosum present and >5 kin lesions Opportunistic infection. Begins as mild pulmonary disease: spreads to local lymph nodes and then quickly to every organ. AIDS px: fever, sweats, weight loss, fatigue, diarrhea, SOB. Pulmonary disease is similar to TB: usually GIT involvement, usually fatal within months. No person to person spread via aerosolized droplets. Unlike othr Borrelia diseases - non relapsing. Tick bite - must stay attached for >48 hrs. 7-30 day incubation. Stage 1: erythema migrans rash "bull's eye lesion". Annular rash with central clearing (40-60% don't get this!) Painless, non-infectious, H/A, myalgia, lymphadenopathy. Resolves 1-2 months. Stage 2: iff untreated develop into neurologic signs (meningitis, Bell's palsy, etc.), conjunctivitis or cardiac dysfunction. Stage 3: 2 months to 2 years after stage 1: migratory arthralgias/arthritis (knees, large joint, TMJ), encephalitis. Resolves in months, years or never. )Can manifest as popliteal cyst. ) If neurologic symptoms: neruoborelliosis.

80

Leptospira interrogenes

Skin / Eye / Liver

Leptospirosis

Range from mild, febrile disease to LV/KI failure (Wei's disease iff icteric) No skin lesion at site of entry. Septic phase: aprupt onset fever, HA, myalgia, nausea, lasts 1 week. Immune phase - two days asymptomatic, then aseptic meningitis with severe HA, NV, myalgia. Weil's disease (icteric) jaundice, scleral and conjunctival hemmorhages and KI failure (MC cause of death)

81

Rickettsia

Skin / Systemic

Rocky Mountain Spotted Fever

Painless tick bite leaves no mark (very low inoculum - <10 organisms) 1 week incubation - rapid fever, severe HA, nausea. 5 days later: rash - diffuse, maculopapular rash, MC spread from trunk to extremities (inclusing palms and soles). Respiratory symptoms. Iff untreated spread to CNS (confusion), SP, GIT, LV. Encephalitis, DIC, shock, death (up to 20% mortality)

Clear yellow discharge (gonorrhea is yellow/purulent) Also termed LGC. MC in Africa, Asia, South America (male homosexuals). Need adequeate sample of infected cells (specimen of pus/ discharge is inapproptirate since they are in the cells). Culture: most specific method, only infects certain cell lines; formation of inclusion bodies. DFA (direct fluorescent) staining. PCR.

Reportable STD. Initial lesion: small painless papule on penis, urethra, glans, scrodtum, vaginal wall. 2nd stage: buboes --> painful, can rupture and drain spontaneously. Systemic. Mimics IBS. Can get proctitis in men and women.

"TB is the master impersonator." Primary infection (only 5% get active TB within 2 years): insidious onset: malaise/ listlessness, night sweats, low grade fever, unexplained weight loss and progressive fatigue. Productive purulent cough progressing to hemoptysis, dyspnea. Apical rales, cyanosis. Secondary TB (reactivation): haematogenous spread anywhere: miliaty TB (no pulmonary signs). Destroys tissues - liver, adrenals...

Unexplained

Difficult: PCR, Microimmunoflorescence Rare person to person spread (nonproductive cough). DX: serology: 4x increase in Ab titre. Prevention: control and quarantine domestic and imported birds.

Low grade

CXR: cavitations in one or more upper lobes of lung. Sputum sample: acid fast bacillus. Fastidious growth requirements, PCR.. Skin test (Mantoux test) - intradermal injection, wait 48 hours and measure induration/ erythema (type IV hypersensitivity). Doesn't tell whether TB is active or not. Will react to skin test - lepromin

Not reactive to skin test

Sputum cultures: acid fast bacilli. CBC with diff: AIDS diagnosis, anemia, neutropenia.

Clinical signs and symptoms and patient history. Culture and IFA stain of biopsy of initial rash (30% don't get rash and cross-reactivity with Treponema). Indirect ELISA. PCR.

Too small for light microscope and Gram stain. Microscopic agglutination.

DDX with Typhoid. (Typhus is Rickettsia). DFA stain of skin biopsy. IFA stain for LPS. Complement fixation tests, (+) iff <4x increase in Ab titer.