E.Coli
Terms
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- Morphology
- related to H. capsulatum
- Virulence factors
-
1.Adhesins
2.exotoxins
3.H (flagella) and K (capsule) antigens
- Virulence factors:
i)special adhesins are sued to attach to the uroepithelium
ii)p-fimbriae
iii)hemolysin enzymes lyse RBC’s, are proinflammatory, resist C-mediated cell lysis - Signs and symptoms
-
-NO GI DISTRESS
-No fever
-Clear sensorium
-Dilated fixed pupils
-Dry / furry tongue
-Bilateral descending weakness of neck, face, throat
-Respiratory paralysis – 32-40% mortality
-No permanent immunity – can get repeated occurrences - lab diagnosis
- pyuria, hematuria, bacteriuria
- exogenous infections
- from contaminated food or water
- Enterotoxigenic (ETEC)
-
-traveler’s diarrhea (Montazuma’s revenge)
-infant diarrhea
-virulence factors
-adhesion factors
-exotoxins
-ST a / ST b ïƒ guanylyl cyclase
-LT 1 / LT 11 ïƒ adenylyl cyclase
-signs and symptoms
-watery diarrhea
-vomiting (rare) - Enteroinvasive (EIEC) (compare Shigella
-
-signs and symptoms include scant, bloody stool that is leukocyte (+), and fever
-might progress to colonic ulceration - Enteropathogenic (EPEC
-
-common cause of infant diarrhea
-signs and symptoms include non-bloody stool, fever, nausea, vomiting - Enteroaggregative (EaggEC)
- -persistent, watery diarrhea, low grade fever, nausea and vomiting
-
Enterohemorrhagic (EHEC)
S/S
V-factors -
-most common strain causing disease in developed nations
-cause of “Hamburger Disease†and HUS
- low inoculation (100 bacilli) is needed
- virulence factors
- verotoxin – destroys GI cells
- ST X – stimulate cytokines to increase virulence and receptor expression
- Hemolysin – central role in disease symptomatology
-signs and symptoms
-bloody diarrhea
-NO fever
-Can progress to HUS
-Spread via undercooked beef or other meat, feces, contaminated water
-HUS
-Most common cause of acute renal failure in children
-Spread
-Person to person (importance of handwashing)
-Signs and symptoms
-Bloody diarrhea
-Acute renal failure (destruction of renal glomeruli)
-Lab diagnosis
-Stool culture (+) for E. Coli O 157:H7
-Hemolytic anemia - Diffuseaggregative (DAEC)
-
- bacteria imbedded in cell membrane of elongated microvilli
-watery diarrhea - neonatal meningitis
-
- most commonly cause by E. Coli and Group B Streptococcus
K1 capsular agonists - Epidemiology
-
-part of the normal GI flora
-increased risk of infection in hospitalized patients and travelers to developed nations
- public hygiene systems in developed nations play a significant role in the rarity of E. Coli infections - Treatment
-
-revent by good personal hygiene
-cook ground beef until the center is brown, not pink, and the juices run clear. The middle of the patty must reach at least 68°C for at least 15 s
-ABC therapy is NOT indicated - SALMONELLA (ENTEROBACTERIACEA, SALMONELLA – family, genus)
- -diseases are gastroenteritis (S. enteitidis) and enteric fever (S. typhi and S. paratyphi)
- S. ENTERITIDIS EPIDEMIOLOGY
-
-poultry / birds
-humans most commonly get salmonellosis from undercooked poultry, contaminated cutting boards, egg salad, undercooked / raw eggs
-disease incidence increases in the summer due to all the BBQ’s
-also more common in children >1 year and elderly > 60 years old - D.S. TYPHI EPIDEMIOLOGY
-
-humans are the only known animal host
-associated with foreign travel – spread by food or water contaminated b infected food handlers (only needs a low inoculum, compare S. enteritidis which needs a very high inoculum) -
SALMONELLA CLINICAL SYNDROMES
-“salmonellosis†regardless of species
-five potential outcomes -
1.no outcome
2.gastroenteritis
-S. Enteritidis – most common cause
-Occurs 6-48 hours after ingestion of contaminated food or water
-Signs and symptoms include: nausea, vomiting, fever
-Most commonly is self limiting
3.Septicemia
-most commonly due to S. typhi, and S paratyphi
-increased risk in AIDS, geriatric or pediatric patients
-symptomology of septicemia is similar to other Gram (-) septicemia (10% of patients develop arthritis, osteomyelitis, and endocarditis)
4.enteric fever
-most commonly spread by food handlers infected with S. typhi (typhoid fever) or S. paratyphoid (paratyphoid fever)
-bacteria passes directly through intestinal walls
-this is NOT typhus which is caused by Rickettsia spp.
-Signs and symptoms include: increasing, remittent fever, rose coloured spots on abdomen
5.asymptomatic carriage – 1-3% - S TYPHI PATHOGENESIS AND COMPLICATIONS
-
-infected foodhandlers - gall bladder - back to intestine to cause increased inflammation
-complications include
-GI lesions: hemorrhage, perforation
-Toxemia: myocarditis, liver and bone marrow damage
-Prolonged serious illness
-Other: menigitis, osteomyelitis, endocarditis - SALMONELLA TREATMENT / PREVENTION, CONTROL
-
-improved personal hygiene and public hygiene
-spread by the 5 F’s: food, fingers, fomites, feces, flies
-avoid antacids (also increased risk of pneumonia)
-clean cutting boards
-most commonly symptomatic treatment instead of ABC’s
-S. Typhus – oral or parenteral vaccine (70% effective, transient immunity, frequent side effects) - SHIGELLA (ENTEROBACTERIACEAE, SHIGELLA – family, genus)
-
-S. flexneri
-Most common cause of shigellosis in developing world
-S. sonnei
-Most common cause of shigellosis in industrialized world
-S. boydii
-S. dysenteriae - PATHOGENESIS
-
- 1° infection – 2-4 days after inhalation ïƒ lymphatics
- 2° viremia – thoracic area, vesiculopapular rah
- VZV becomes latent in DRG or cranial root ganglia -> reactivated in older adults and immunocompromised >dermatome ->shingles - CLINICAL SYNDROMES
-
-simple wound infection
-anaerobic cellulitis
-subcutaneous tissue – spares fascia and deep muscles
-superficial skin discoloration and skin necrosis
-gas forms -suppurative myositis – foul smelling discharge
-no muscle necrosis
-NO systemic S/Sx
-myonecrosis (gas gangrene)
-rapidly worsening of cellulitis
-trauma - intense pain, extensive muscle necrosis (blue black, edematous, does not bleed or contract on stimulation), toxic delirium
-much damage due to alpha toxin an gas bubbles
-diagnosis:
- debridement
-gram (+) rods in tissue specimens with no leukocytes
-food poisoning (#4 - #1 Campylobacter jejuni, #2 salmonella, #3 S. Aureus)
-from meat – refrigeration and re-heating destroys enterotoxins (compare B. cereus heat labile toxin that causes diarrhea)
-large infective dose needed
-abdominal cramps
-watery diarrhea
-NO fever
-NO nausea or vomiting - VIBRIOACAE, VIBRIO – family, genus, species
-
-V. parahemolyticus
-V. vulnificus
-V. Cholera (most known)
-200 serotypes
-EI tor biotype is most common in world today - VIRULENCE FACTORS (V. Cholera)
-
1.cholera toxin complex A-B toxin:
-structurally and functionally similar to heat – labile enterotoxin A of E. coli
-B toxin
-A toxin
-Increase cAMP
-Cause electrolyte shift - watery diarrhea
2.Adhesins
-strong attachment to intestinal epithelium despite peristalsis and flushing
3.Mucinase (hemagglutination protease)
-intestinal inflammation and degradation of tight junctions
4.Siderophores
-sequester iron
5.Neuramidase
-increase toxin receptors (compare influenza)
6.Hemolysin
-hermostable
-increase intracellular Ca -increase chloride secretion - EPIDEMIOLOGY (V. Cholera)
-
-ubiquitous in marine environment (contrast salmonella and campylobacter)
-even in increased salinity and temperature (10°C to 30°C)
-contaminated shellfish / seawater is most common way to transmit disease (compare Hep A)
-asymptomatic human carriers in endemic areas also transmit disease
-relatively infectious (contrast Shigella – especially if normal acidity)
-most cases seen in returning travellers(compare enterotoxogenic E. Coli) - CHOLERA S/S
-
-abrupt onset of watery diarrhea and vomiting
-rice water stools – colorless, odorless, no protein, speckled with mucus
-severe fluid and electrolyte loss – dehydration, metabolic acidosis, hypokalemia
-NO ABDOMINAL CRAMPS
-NO FEVER (contrast Shigella, Salmonella, Campylobacter)
-Resembles ETEC induced gastroenteritis - CHOLERA LAB DIAGNOSIS
-
-rarely seen in gram stained stool or wound specimens
-dark field / phase contrast microscopy – characteristic darting motility
-direct ELIZA - CHOLERA TREATMENT, PREVENTION, CONTROL
-
-aggressive fluid / electrolyte replacement (oral / IV) reduces mortality to less than 1%
-no long term human carriers (contrast S. typhi)
-vaccine – limited usefulness due to short lived protection - BACILLACEAE, BACILLUS – Family, genera
-
- Gram (+) bacillus
- Endospore forming
- 2 main species that cause disease in humans
-B. anthracis – anthrax
-B. cereus – gastroenteritis (contaminated “cereal,â€rice) - B. ANTHRACIS
-
-biological warfare
-Gram (+) bacillus
-Clinical samples – single or paired – “jointed bamboo-rodâ€
-Culture – long serpentine chains “medusa head†- CUTANEOUS ANTHRAX
-
-transmission: break in skin exposed to spores which can survive for years
-diagnosis:
-history: mail carrier; painless, necrotic eschars
-lab diagnosis: Gram (+) bacillus in lesions, NO neutrophils
-other: internal hemorrohage
-Vs. ORF
-B. anthracis (pox virus)
-Direct contact with spore contaminated with animal products (direct contact with infected sheep or goat)
-Painless papule with necrotic eschar and gelatinous edema (painless vesicles – red weeping nodules)
-Arms, hands face, neck (hands)
-Potentially fatal – 20% (benign and self limiting) - INHALATION ANTHRAX
-
-carried by alveolar macrophages to mediastinal lymph nodes – prolonged latency
-initial disease
-fever / chills
-dyspnea
-cough
-head ache
-vomiting
-chest / abdominal pain
second stage
-rapidly worsening fever
-diaphoresis
-pulmonary edema
-massive enlargement of mediastinal lymph nodes
-shock - death with in 3 days
-hemorrhagic meningitis symptoms (more common than pulmonary symptoms) - INGESTION ANTHRAX
-
-Upper GI
-Oral / esophageal ulcers
-Edema
-Sepsis
-Regional lymphadenopathy
-dysphagia
Lower GI
-Nausea
-Vomiting
-Malaise
-Systemic S/Sx
-Bloody diarrhea
-Rare but almost 100% mortality - TREATMENT / PREVENTION
-
-ABC’s are of limited use (disease is not recognizable until peak infectiousness has passed)
-Prevention: DPT vaccine – 2,4,6,15 months and 4-6 years
-Now use acellular B. pertussis (DtaP) (“fewer side effectâ€) - B. CEREUS
-
-low mortality compared to B. Anthracis
-causes two types of gasteroenteritis
1.emetic disease
-heat stable enterotoxin
2.diarrhoeal disease
-heat labile enterotoxin
-also causes panopthalmitis which is inflammation of the entire eye after a traumatic injury (also caused by S. aureus, Candida albicans, S. pneumonia, E. coli, N. meningitidis) (compare keratitis due to pseudomonas) - FOOD BORN DISEASE
-
a)emetic disease
-NO FEVER
-NO DIARRHEA
b)diarrheal disease
-nausea
-bloody diarrhea
-NO FEVER - PANOPTHALMITIS
-
-post traumatic
-rapid (<48 hours) - TREATMENT AND PREVENTION
-
currently no longer using penicilin due to resistance – beta lactamase, need to hight dose, damage cell surface so ABC can’t penetrate cell
- prevention: safe sex - CAMPYLOBACTERACEAE (Family)
-
-small (0.3-0.6 um) – filterable unlike other bacteria
-Gram (-) bacillus – S or gull-wing shaped
- Motile – single bipolar flagella (compare V. cholera)
- Microaerophilic (can survive on decreased oxygen and increased carbon dioxide)
-Thermophilic (42°C) - CAMPYLOBACTER JEJUNI GASTEROENTERITIS
-
-need high infectious dose
-reduced with hypochloridria, TUM’s and milk
-2-11 day incubation
-foul smelling, watery diarrhea - profuse bloody diarrhea
-NO VOMITING
-Resolution in 3 days to 3 weeks
-Residual histological damage to GI mucosa (compare EIEC, enterolytictia? E. coli and shigella shiga toxin) - GUILLIAN BARRE SYNDROME
-
-due to many causes: C. jejuni enteritis, immunizations, pregnancy, etc…
-idiopathic, peripheral polyneuritis 1-3 weeks after the above mild condition
-progressive, symmetric pain and weakness in extremities – might ascend to trunk, face, thorax
-self limiting (few weeks to few months) with complete recovery
-autoimmune? - HELICOBACTER PYLORI
-
-Gram (-) bacillus – but gram stain is variable (spiral in fresh culture, coccoid in older culture)
-Motile – flagellated – “corkscrew motionâ€
-Urease (+) - breaks down urea to amonia and something else which increases the pH - surrounded by buffer cloud which allows it to survive in the stomach
-Temperature 30°C-38°C (contrast Compylobacter spp.) - COLONIZATION FACTORS
-
-survive acidity
-acid inhibitory protein
-urease
-flagella
-mucinase – breaks down mucin layer in stomach
-phospholipase
-microaerophillic
-survive in relatively anaerobic environment of stomach - DISEASES
-
-opportunistic infection
-begins as mild pulmonary disease and spreads to local lymph nodes and then quickly to every organ
-AIDS patients show fever, sweats, weight loss, fatigue, diarrhea, SOB
-Pulmonary disease is similar to TB
-Usually GIT involvement
- Usually fatal with in months
- No person to person spread via aerosolized droplets - CLOSTRIDIUM SPP (BACILLACEAE – family)
-
-Gram (+) bacilli
-Most commonly anaerobic
-Spore formers
-3 general classes
-histotoxic – C. perfringen
-enterotoxigenic – C. difficile
-paralytic – C. tetani, C. botulinum - C. PERFRINGENS
-
-gram (+) “plump, rectangular†rod
-causes wound / soft tissue infections
-non-motile but rapid growth on sheep’s blood agar (use to distinguish)
-5 Toxins – Type A: permanent soil inhabitant, responsible for most human disease - PATHOGENICITY
-
-spore formation – long term survival
-alpha toxin – most tissue damage – vascular permeability increases, lyses cells
-heat kills enterotoxin - Lab DX
-
-patient history
-clinical S/Sx
-gram stain and culture not that important because only 30% of people with tetanus are culture (+) - C. DIFFICILE
-
-can be a normal part of GI flora without causing disease (3% will have with out disease)
-most commonly causes post ABC diarrhea and pseudomembranous colitis - TREATMENT & PREVENTION
-
-acid pH (canned fruit is ok) – grow best at pH < 4.5 ??
-refrigerate (can’t survive < 4°C)
-heat for a minimum 10 minute at 80°C
-no honey to infants < 1 year old
-check cans – swollen - C. TETANI “extreme tensionâ€
-
-gram stain variable (compare helicobacter pylori)
-classic “tennis racketâ€
-very sensitive to oxygen – obligate anaerobe
-relatively inactive metabolically (contrast C. perfringens) - GENERALIZED TETANUS
-
-later signs: opisthotonus – back arching most common form of tetanus
-bacterium introduced by trauma to skin – animal bites
-early signs: exaggerated deep tendon reflexes, trismus (lock jaw) – masseter muscle, risus sardonicus (mock smile), drooling - OTHER FORMS OF TETANUS
-
-localized
-cephalic
-neonatal – from improperly cleaned umbilical stump
-firs sign: difficulty sucking 8-10 days after birth - C. BOTULINUM
-
-gram (+) bacillus “sausage shapedâ€
-produces one of the most potent exotoxins know to humans
-ubiquitous – sediments of lakes and ponds - FOOD BORNE BOTULISM – INTOXICATION
-
-inadequate sterilization of food – home canned foods, preserved fish
-2-72 hours incubation - INFANT BOTULISM – INFECTION, INTOXICATION
-
-honey contaminated with spores (pacifier)
-most common form of botulism in USA
-most common in 1-6 month olds due to bacteria growing and producing neurotoxin in infant GIT, and infant GIT doesn’t have as many competitive bowel microbes - S/Sx
-
-Non specific – constipation, weak cry, failure to thrive, weak suckling
-Floppy baby – acute flaccid paralysis (head, face, throat descending to extremities)
-Death from respiratory paralysis – low mortality (1-2%) - NEISSERIA
-
-gram (-) diplococci “coffee beanâ€
-transparent colonies on chocolate blood agar -
-N. meningitidis
-Normal colonizer of nasopharynx or cause disease - -asymptomatically colonize nasopharynx or cause meningitis, meningococcemia or pneumonia
- MENINGOCOCCEMIA
-
marked disease
-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)
-If untreated can progress to disseminated intravascular coagulation or hemorrhage into adrenal glands
-Sequelae
-none or large areas of necrosis / skin ulceration (skin grafts)
-deafness (affect CN VIII) or squint (affect CN VI) - MENINGOCOCCAL MENINGITIS
-
-N. meningiditis is 2nd M/C cause of adult bacterial meningitis
-Triad of rapid onset of fever, nuchal rigidity, blinding headache
-Hight number of gram (-) diplococci organisms in PMN of CSF
- inflammation of membranes covering the brain and spinal cord (M/C’ly caused by N. meningiditis, H. influenza, S. pneumonia)
-modes of control
a)proper hygiene
b)good diet (immune supporting)
c)polysaccharide vaccine
d)avoid close contact with intected person
e)ABC’s -
-N. gonorrhoeae
Strict pathogen -
A.N. GONORROEAE
-“the gonococcuâ€
-gram (-) diplococci
-fastidious growth
-2nd most common STD in USA (chlamydia is #1) -
PATHOGENESIS
v-factors -
-no exotoxin – host damage is from gonococcal induced inflammatory response
-anti-phagocytic – negatively charged capsule
-Pili – tissue tropism: non-ciliated epithelial cells of foreskin, vagina, fallopian tube
-LOS – classic endotoxin activity (like LPS)
-Fe++ binding proteins
-IgA protease
-Beta lactamase (degrades penicillin - GONORRHEA IN MALES
-
-95% of men get acute symptoms (most commonly gonococcal urethritis)
-infection usually restricted to mucosa of penis
-2-7 day incubation – purulent urethral discharge, red / edematous urethral meatus
-can progress to peri-uretrhal abcesses, prostatitis, epididymitis - GONORRHEA IN FEMALES
-
- >50% of women are asymptomatic carriers or have mild symptoms (cervicitis)
-iff acute: vaginal discharge, and abnormal vaginal bleeding
-if untreated - ascending infection - major cause of infertility - DISSEMINATED GONORRHEAE
-
-rare but M/C in women (1-3%)
-S/Sx: fever, migratory arthralgias, tender papillary lesions / rash on the extremities
-Arthritis: M/C’ly mono-articular – knee in females
-N. gonorrhoeae is the #1 cause of purulent arthritis in young adults - HAEMOPHILUS SPP. (blood loving)
-
-small, gram (+) coccobacillus
-pleomorphic (many sizes and shapes
-fastidious growth requirements
-X factor (hematin) and V factor (NAD)
-obligate parasites on mucous membranes of humans and animals
-2 main species: H. influenzae and H. Ducreyl - A.HAEMOPHILUS DUCREYL
-
-small, gram (-) coccobacillus
-non-encapsulated - CHANCROID
-
H. ducreyi
Soft, purulent, painful ulcer (genitalia)
MC in uncircumcised males tropical and sub-tropical (female – carrier)
5-7 day incubation
ïƒ painful buboes (swollen inguinal lymph nodes), phimosis (can’t pull foreskin back over shaft of penis), urethral structure
dyspaerunia (painful intercourse in females)
Gram (-) coccobacillus - PRIMARY SYPHILIS
-
Treponema pallidum
Hard, non-purulent, non-painful ulcer
Both sexes 20-35 yoa
3 week incubation
ïƒ painless buboes
Poor gram stain – dark field microscopy (spiral rods, thin tightly coiled), non-specific tests (VRDL, RPR), specific tests (FTA-Abs, TPHA) - HAEMOPHILUS INFLUENZAE
-
-non-encapsulated strains colonize both upper and lower respiratory tracts
-encapsulated strains (serotype b) can become systemic - LAB DX, TX, CONTROL
-
-Gram stain of CSF (for meningitis only), blood (other diseases)
-Culture on chocolate agar
-Immunology – agglutination reaction for PRP capsule in CSF and urine
-Treatment – ampicillin, broad spectrum cephalosporins
-Control – conjugated HiB vaccine (purified PRP) – effective against encapsulated strains only – still get OM, cellulitis
-HbOC at 2, 4, 6, 15 months or
-PRP-OMC at 2, 4, 12 months - BORDETELLA SPP.
-
-gram (-), very small bacilli (rodlike)
-fastidious growth
-humidity, specialized media: charcoal, blood, NAD-enriched
-B. pertussis - whooping cough - WHOOPING COUGH
-
-incubation – 7-10 days
-catarrhal (mucus) – 2 weeks, looks like common cold: rhinorrhea ***MOST INFECTIOUS STAGE
- paroxysmal stage – 1-2 weeks, dry non-productive, repetitive “whooping†cough
-convalescent stage – 2-4 weeks - TREPONEMA PALLIDUM
-
-Treponema, Spriochaetalis (family, order)
-Small, thin, coiled spirochetes – can’t visualize via gram stain and light microscopy
- Motile – “cork screw†motility via thin fibrils at both ends
-Strict human pathogen - SUB SPECIES PALLIDUM EPIDEMIOLOGY
-
-humans are the only reservoir of disease
-syphilis (lover of swine) 3rd MC STD in USA (#1 Chlamydia, #2 Gonorrhea)
-very labile, susceptible to drying (can’t get from toilet seat, or dry skin)
- contagious only during primary stage and rash of secondary stage - SUB SPECIES PALLIDUM VIRULENCE FACTORS
- SUB SPECIES PALLIDUM VIRULENCE FACTORS
- SYPHILIS
-
1.Primary
-small papule – painless, hard chancre
-painless, regional lymphadenopathy – buboes
-very infectious (exudes fluid loads with spriochetes)
-heals spontaneously with in 2 months with out scarring
2.Secondary
-flu-like syndrome
-localized lymphadenopathy
-diffuse, non-pruritic maculopapular rash (includes soles, palms) – very infectious
-resolves slowly in weeks to months
3.Tertiary (Lues / leutic)
-after 3-40 years of latent syphilis
-neurosyphilis
-cardiosyphilis
-painless or deep burrowing pain
4.Congenital
-infected mother infects infants
-born appearing well then several weeks or up to 2 years later – snuffles, widespread desquamating maculopapular rash - TX, PREVENTION, CONTROL
-
-hygiene (spirochetes destroyed by soap and water, temperature >42°C and drying
-safe sex practices - FAMILY CHLAMYDIA
-
- Very small gram (-) bacillus with virus and bacteria like properties
- Unlike other bacteria, there is no PG layer, therefore no gram stain
- Unique growth cycle within host cell – elementary bodies (extracellular survival and initiation of infection), and reticulocyte bodies (adapted for intracellular growth; metabolically active)
-Inclusion body – high amount of glycogen, therefore stain with iodine (DIAGNOSIS)
- 2 separate genera
1.Chlamydia trachomatis
2.Chlamydophila psittaci, and C. pneumonia - PATHOGENESIS, IMMUNITY (Chlamydia trachomatis)
-
-gains access through minute abrasion or lacerations
-limited tissue tropism: non-ciliated epithelial cells of mucous membranes of urethra, endocervix, endometrium, fallopian tubes, respiratory tract, conjuctiva
-strains causing LGV can cause systemic infections by entering lymphatic system
-clinical S/Sx due to direct destruction of cells during replication and host inflammatory response
-no long-term immunity - TRACHOMA (chronic follicular keratoconjunctivitis) EPIDEMIOLOGY
-
-leading cause of preventable blindness in developing countries
-MC in children
-Poor hygiene (no access to water, but they are clean people)
- Spread by droplets, hands, contaminated clothing, eye make-up, flies - TRACHOMA DISEASE
-
-must have specific attachment to conjunctiva-resist flushing from tears
-begins as conjunctivitis
-entropion – eyelashes chronically irritate cornea - TRACHOMA INCLUSION CONJUNCTIVITIS
-
1.Adult
- MC 18-30 yoa and sexually active
- Genital infection first and then unilateral mucopurulent discharge in eye
2.Neonatal
- bilateral, intense papillary conjuctivitis with lid swelling (compare nisseria) - CHLAMYDIA UROGENITAL INFECTIONS
-
-currently MC bacterial STD in USA
1. Women
-termed chlamydia (the drip)
-MC’ly assymptomatic
-Pain / cramping in lower abdomen, dyspaerunia, bleeding between menses
2. Men
-termed NGU (non gonococcal urethritis)
-MC symptomatic
-Yellow, clear discharge
-Pain / tenderness of genitals
-Reactive arthritis - REACTIVE ARTHRITIS
-
-Seronegative spondyloarthropathy
-MC in young men (20-40 yoa that are HLA-B27 positive
-C. trachomatis is MC bacterial pathogen
-S/Sx: unexplained diarrhea, superficial lesions on palms / soles / oral mucosa - LYMPHOGRANULOMA VENEREUM EPIDEMIOLOGY (LGV)
-
-MC in Africa, Asia, South America in male homosexuals
-STD
-Initial lesion
-Small painless (compare syphilis, contrast everything else) papule on penis, urethra, glans, scrotum, and vaginal wall
-2nd stage
-painful buboes which can rupture and drain spontaneously
-systemic
-can get proctitis (anal inflammation) in men and women - CHLAMYDIA TRACHOMATIS LAB DX
-
-Need adequate sample of infected cells (specimen of pus / discharge is anappropriate)
-Culture: most specific method, only infects certain cells lines; inclusion bodies
-Direct fluorescent antibody staining - CHLAMYDIA TREATMENT, PREVENTION, CONTROL
-
-MC also have presumptive Tx for gonorrhea
-Hygiene (hand / face washing)
-Safe sex practices - CHLAMYDOPHILA PNEUMONIA
-
-human pathogen that can cause atypical pneumonia (mild, persistent cough / malaise that might progress to lobar pneumonia)
-potential risk to atherosclerosis, MS, alzheimer’s? - CHLAMYDOPHILA PSITTACI
-
-cause psittacosis
-risk from psittacine birds (parrots, macaws, parakeets, cockatils)
inhaled dried bird excrement, urine and respiratory secretions - PSITTACOSIS DISEASE
-
-non-productive cough
-commonly progresses to CNS
-prevented by controlling and quarantining domestic and imported birds - MYCOBACTERIUM
-
-look fungal when initially growing
->70 spp. And many are associated with human disease
-M. tuberculosis, M. lepra, M. avium Complex
-Runyon classification depending on growth characteristics and pigments produced with light
-Acid fast bacillus (mycolic acid resists acid so binds strongly to stain) -DIAGNOSIS
-One of the slowest dividing microorganisms (life cycle is 18-24 hours so ABC are needed for long time)
-Mycolic acid in cell wall – acid fast, resists drying, detergents, acids / bases
-PPD for mantoux test -
M. TUBERCULOSIS
EPIDEMIOLOGY -
-cause of more fatalities worldwide than any other infectious disease
-MC’ly in person to person transmission via infectious aerosolized particles (which can stay in a room for 45 minutes)
- Very small inoculum needed (as little as 1-3 organisms)
- Increased risk in SE, Asia, Eastern Europe, Northern Mexico, sub-Saharan Africa in immunocomprimised patients - DISEASE
-
-two main types of human disease depending on the host immunity
1.Tuberculoid (Paucibacillary) – “sparce†less infectious & skin lesions
-not infectious
-< 5 cutaneous macular lesions w/ hypopigmented centres
-will react to skin test - lepromin
2.Lepromatous (Multibacillary) – “many†more infectious and more skin lesions
-highly infectious
-most destructive – disfiguring skin / bone / cartilage lesions (“leonine facesâ€)
->5 skin lesions - TREATMENT, PREVENTION, CONTROL
-
- Denver protocol: multi-drug cocktails for >3-6 months
-Problem: MDR-TB
-Diet/robust immune system -
M.LEPRAE
EPIDEMIOLOGY -
-similar structure as M. tuberculosis but can not be artificially cultured (need live mice or armadillos) and grow in Globi bundles
- rare in USA
-Armadillos are natural reservoir
-Spread via respiratory route or contact with break in skin -
AVIUM INTRACELLULARE COMPLEX
EPIDEMIOLOGY -
-opportunistic infections mostly affecting HIV / AIDS patients
-lymphadenitis
-ubiquitous in water and soil
-transmission via ingestion (raw fish / hard cheese / water) and inhalation - DIAGNOSIS / TREATMENT
-
-sputum cultures / smears: acid fast bacilli
-CBC w/ differential diagnosis: AIDS diagnosis, anemia, neutropenia
-Liver function tests: elevated AST / ALT
-Imaging: CT scan
-Chest: medinastinal lymphadenopathy
- Abdomen: lymphadenopathy, and hepatomegaly and splenomegaly
- ABC: clarithromycin, azithromycin, ethambutol, rifabutin - Fungal morphology
-
1. filamentous
-molds (mycelium)
-M/C at lower temps and free living
2. Unicellular
-yeasts
-M/C at higher temperatures and when parasitizing tissue -
fungal disease classification
1.superficial -
-infect outer most (dead) layers of skin
-no immune response
-eg: piedra / trichosporosis
-BLACK piedra (scalp, mustache, beard, groin)
-D/t direct or sexual contact
-Ddx: dark, hard nodules along infected hair shaft
-WHITE piedra (scalp)
-Directed contact
-Ddx: soft, pasty white growth on hair shaft
-eg: tinea (pitryiasis) versicolour
-Malasseiza furfur
-non-itchy, hypo-pigmented lesions on upper torso, arms abdomen
-ddx: “spaghetti and meatballs†organism after KOH prep and woodlamp’s positive
-eg tinea nigra
-Phaeoannuellomycose wernickii
-Well demarcated macular lesions on palms and soles
-Ddx: dark pigmented yeast cells - 2.cutaneous
-
-infect deeper layers of epidermis, hair, nails
-invoke inflammatory immune response
-caused by 3 main genera – mistakenly termed dermatophytes
-eg: most tineas
-ddx: woods lamp (+) - 3.submucotaneous
-
-infects the dermis and subQ tissue (fascia, muscle, bone) following tissue trauma
-rare in developed countries
-might be difficult to treat
-eg: lymphocutaneous sporotrichosis - 4.systemic
-
-invades internal organs esp LUNG foci (respiratory tract as initial foci of infection)
-M/C’ly develop mild acute / asymptomatic lung infections
-Can also develop chronic diease or sub – clinical (latent)
-eg: histoplasmosis, blastomycosis, coccidioidomycoses - SYSTEMIC MYCOSES
-
-mycotic agents can cause disease in humans and are either:
-strict pathogens
-Histoplasma capsulatum
-Blastomyces dermatitides
-Coccidiodes immitis
-opportunistic pathogens
-Candida albicans
-Aspergillus flavus
-Cryptococcus neoformans - HISTOPLASMA CAPSULATUM
-
-saprobic phase
-in N2 rich soil
-parasitic phase – thermal dimorphism
-in macrophages of Reticular Endothelial System / Mononuclear Phagocytic System - HISTOPLASMOSIS (darling’s disease, cave / spelunker’s disease)
-
-primary histoplasmosis (5% of people):
-10 d incubation
-acute, self limiting influenzae like illness
-residual calcified lesions in LU and lymph nodes
-not contagious
-complications
-overly aggressive immune response -> Mediastinal fibrosis - ocular histoplasmosis syndrome:
-
-serious retinal condition – leading cause of blindness in 20-40 yo
-“histo spots†bilaterally
-M/C’ly no visual loss but can be activated to cause visual changes like:
1.sub-retinal neovascular membrane – abnormal blood vessel growth or fluid leak into macula - severe scarring and vision loss
2.metamorphosia – wavy distorted vision due to stretching / distortion of retina
3.decreased central vision acuity – blind spot
4.others
-progressive -> disseminated via lymphatics (increased risk if impaired T-cell mediated immunity)
- TB-like: fever, night sweats, weight loss w/ destructive (caseating necrosis) lung lesions - BLASTOMYCES DERMATIDES
- related to H. capsulatum
- BLASTOMYCOSIS
- gilchrists disease, chicago disease
- acute
-
-bronchopneumonia
-***drenching sweat
-no residual calcified lesions (unlike histoplasmosis)
-not contagious - chronic
-
-TB or cancer like
-Skin lesions: slowly expanding ulcerative or verrucous lesions on face, nose and mouth - COCCIDIODES IMMITIS
-
-dimorphic
-37°C, tissue, mulitnucleated spherule “sporangiaâ€
-new world disease – NA
-endemic in soils of hot, dry, semi-arid areas
-spread via dusty storms
-M/Cly in males 25-55 yo -
COCCIDIODOMYCOSIS (
san joaquin valley fever, desert rhematism, posade-wernicke disease) -
-inhalation of conidia
-M/Cly asymptomatic
-40% mild, febrile to moderately severe respiratory disease
-not contagious
-<5% - progressive pulmonary diesase
-<<1% - disseminated disease erythema nodosum w/ arthralgia - DIAGNOSIS
-
- tzanck smear – giant, multinucleate cells – synctia (compare parameso viruses, HSV, HIV, VZV)
-cowdry type A inclusion bodies – drop like masses of acidophillic material surrounded by a clear halo with in the nucleus -
BASIC VIRAL STRUCTURE
VIRION - whole virus particle
- CAPSID
- protein coat surrounding the genome – many different shapes and sizes -> involved in packaging, protection and enzymes
- NUCLEOCAPSID
- genome, structural proteins and capsid
- VAP’s (viral adhesion protein
- surface glycoproteins on capsid or envelope -> binding to specific cells, Ags for protective immunity, enzymatic, cell fusion etc (lose evelope, lose attachability)
- HEMAGGLUTININS
- specialized VAP that binds to RBC’s
- ENVELOPED VIRUS
-
Fragile
Must remain wet
Labile to acids / detergents
Spread b/w cells
Pathogenesis dt hypersensitivity and inflammation - NAKED CAPSID VIRUS
-
Robust
Survive some drying
Resistant to acids(ST acid), detergents (bile)
Spread by lysing cells
Pathogenesis dt host cell lysis - VIRAL DISEASE
- Acquisition entry – inhalation
- Initiation of infection
-
Incubation period – amplification and spread to 2° site via blood (viremia) or lympathics
Potential outcomes include: asymptomatic, non-specific early signs (prodrome) or systemic / local damage directly (virus) or indirectly (immune system) - Covalescence
- body repairs damage and develops immunity to protect self in future
- VIRAL IMMUNITY
- Immune system (cell mediated immunity and humoral immunity) is the best and often only means of controlling a viral infection
- Interferon
-
-systemic symptoms (fever)
-activate immune system
-warn neighboring cells - NK cells
-
-kill “Ab-tagged†infected cells and tumor cells (Ab Directed Cellular Cytotoxicity)
-stimulate IFN gamma - T cells
-
-CD4TH – activate CTL’s
-CD8 – (CTL’s)-> kill infected cells and therefore, eliminate source of new viruses - Ab
- block spread of extracellular virus to other cells
- HERPESVIRIDAE FAMILY
- - group of 8 DNA viruses grouped together dt their common virion morphology and mode of replication
- 3 sub families
-
-alpha – HSV-1, HSV –2, VZV
-beta – CMV, HHV-6, HHV-7, HHV-8
-gamma – EBV - replication
-
-adherence – interaction w/ viral glycoproteins and host cell surface receptors
-entry – envelop fuses w/ host cell plasma membrane and nucleocapsid enters cytoplasm
- transport to nucleus – nucleocapsid fuses w/ nucleus and DNA enters
- replication – virus encoded DNA polymerase
-lytic infections of fibroblasts / epithelial cells inhibit host cells of DNA and mRNA synthesis, degrade host DNA to use as substrate for its own replication (nasty buggers)
- outcomes
- latent infections – of neurons only
-persistent infections
-immortalizing infections - -TRANSMISSION: 4 M’s
-
Mixing & Matching of Mucus Membranes
- HSV-1: transmitted early in life via oral contact or autoinoculation (self – eg: eye to mouth)
- HSV-2: transmitted later in life
- Horizontal: person to person via sexual practices
-Vertical: mother to child via ascending in utero infection or during vaginal - INFECTION:
-
-Skin break
-Localized 1° infection in mucosa -> vesicular lesions ->retrograde transport ->stress (emotional, fever, direct sunlight, menstruation / hormones, immunosuppression) - ORAL HERPES (HERPES SIMPLEX, HERPES GINGIVASTOMATITIS)
-
-dew drop on rose petal -> pustules, shallow ulcers and then crust over w/ yellowish crust
- 2° infection is less severe, more localized and shorter duration than 1° infection - HERPES CLINICAL SYNDROMES
-
-HERPETIC KERATITIS (ocular herpes) –> corneal ulcers -> permanent blindness (compare pseudomonas causing blindness in contact wearers)
-HERPETIC WHITLOW – herpes infection of finger / wrists (of health professionals attending to HSV px) - HERPES SIMPLEX CNS INFECTIONS
-
-MENINGITIS – HSV-2: nuchal rigidity, blinding HA, nausea, photophobia
-ENCEPHALITIS – HSV-1: seizures, signs of Space Occupying Lesion -> destruction of temporal lobe (learning memory)
-Most common cause of sporadic encephalitis - GENITAL HERPES
-
-caused by HSV-1 (10% dt orogenital sexual practices) and HSV-2 (90% dt genital to genital contact)
-STD 3-7 days after contact
-Regional lymphadenopathy
-painful (compare chanroid ulcers, contrast syphillis ulcers), shallow ulcers
-Recurrent – prodrome of burning / tingling - FEMALE
-
- pruritis
- vaginal or cervical mucoid discharge
-increased risk of cervical CA in adulthood - MALE
-
-Dysuria
-Dyspaerunia - NEONATAL HERPES SIMPLEX INFECTION
-
-acquired in utero or during vaginal birth or post natally (family members or hospital personnel)
-devastating often fatal - CONTROL
-
-avoid contact w/ mucocutaneous lesions – infections from prodrome even to crusted lesions
- pregnant women – c-section if active genital herpes
-strengthen immune system, avoid triggers - VARICELLA ZOSTER VIRUS
-
-don’t confuse varicella w/ variova (small pox)
-AKA herpes virus III
-cause of chicken pox (aka varicella) and shingles (aka herpes zoster)
- like herpes simplex:
- blister-like lesions (but different sizes and stages, deeper, more painful and can cause scarring)
- latent infections
- cell mediated immune system plays a big role in controlling infections
- unlike herpes simplex:
- spreads predominantly via respiratory route
-no detectable lesions at site of entry - CHICKEN POX
-
-one of the 5 childhood exanthems (eruptions) amongst rubella, roseola, 5th disease, measles / rubeola
-macuopapular rash (dew drop on rose petal)
-intense pruritis
-spread from back / chest to scalp, face and extremities – rarely on soles and palms
-successive crops of lesions
-much more harmful to adults – overzealous CMI will cause more extreme cell damage, interstitial pneumonia, CNS involved, scarring
-chicken pox rash is more severe on trunk than extremities – also on mouth, conjunctiva, vagina - CHICKEN POX COMPLICATIONS
-
° bacterial infection
2.reyes syndrome
-1 week after acute viral: exanthematous rash, severe vomiting
-2 days later: CNS symptoms
-can occur after chicken pox, enterovirus, EBV, influenzae B, aflatoxin, pesticide
-increased risk if < 18 yoa
-pathology unknown
ASA associated – DO NOT give ASPIRIN to a child w/ chickenpox - HERPES ZOSTER – shingles
-
-recurrence of latent VZV infection dt stress
-Prodrome – severe pain in localized nerve area
-3-5 days later – gradual development of small red macules, closely spaced. Most commonly in thoracic area or trigeminal nerve area – UNILATERAL
-post herpetic neuralgia – long term (months to years) severe recurring burning or itching pain, hyperesthesia
-unlike herpes simplex – lesions are various sizes - SHINGLES COMPLICATIONS
-
-herpes zoster opthalmicus – CN V, III
-ramsay hunt syndrome (herpes zoster oticus) – painful lesions along CN VIII (severe otalgia, hearing loss, vertigo), CN V - VZV TX and CONTROL
- relatively mild disease that gives life-long immunity