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216 Cards in this Set
- Front
- Back
Morphology
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- Gram (-) bacillus with outer envelope (subject to drying)
-O antigens used for strain typing (O157:H7) |
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Virulence factors
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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 |
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Signs and symptoms
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i) Cystitis
- dysuria, urgency, increased frequency, incomplete voiding ii) pyelonephritis - same as cystitis but more severe and with fever, loin pain and (+) KI punch Septicemia - E. coli causes 45% of enterobacterial septicemia |
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lab diagnosis
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pyuria, hematuria, bacteriuria
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exogenous infections
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from contaminated food or water
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Enterotoxigenic (ETEC)
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-traveler’s diarrhea (Montazuma’s revenge)
-infant diarrhea -virulence factors -adhesion factors -exotoxins -ST a / ST b guanylyl cyclase -LT 1 / LT 11 adenylyl cyclase -signs and symptoms -watery diarrhea -vomiting (rare) |
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Enteroinvasive (EIEC) (compare Shigella
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-signs and symptoms include scant, bloody stool that is leukocyte (+), and fever
-might progress to colonic ulceration |
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Enteropathogenic (EPEC
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-common cause of infant diarrhea
-signs and symptoms include non-bloody stool, fever, nausea, vomiting |
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Enteroaggregative (EaggEC)
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-persistent, watery diarrhea, low grade fever, nausea and vomiting
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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 |
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Diffuseaggregative (DAEC)
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- bacteria imbedded in cell membrane of elongated microvilli
-watery diarrhea |
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neonatal meningitis
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- most commonly cause by E. Coli and Group B Streptococcus
K1 capsular agonists |
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Epidemiology
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-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 |
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Treatment
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-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 |
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SALMONELLA (ENTEROBACTERIACEA, SALMONELLA – family, genus)
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-diseases are gastroenteritis (S. enteitidis) and enteric fever (S. typhi and S. paratyphi)
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MORPHOLOGY
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-Gram (-) bacillus
-Outer membrane – so susceptible to drying |
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VIRULENCE FACTORS
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1.Surface antigens
a)O Ag (on LPS) b)V1 Ag (on capsule) c)Species specific fimbria attach to M cells on peyers patches 2.Endotoxin -responsible for the fevers (IL-1 signal to hypothalamus) 3.Invasiveness -penetrate into sub-epithelia spaces with out a toxin mediated process – rearrange the host cell actin (membrane ruffling) 4.Enterotoxins a)LT / ST-like toxins (compare E. Coli) b)Ditto c)Verotoxin like 5.Other -Acid tolerance response gene -Catalase -SOD |
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S. ENTERITIDIS EPIDEMIOLOGY
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-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 |
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D.S. TYPHI EPIDEMIOLOGY
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-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) |
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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% |
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S TYPHI PATHOGENESIS AND COMPLICATIONS
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-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 |
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SALMONELLA TREATMENT / PREVENTION, CONTROL
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-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) |
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SHIGELLA (ENTEROBACTERIACEAE, SHIGELLA – family, genus)
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-S. flexneri
-Most common cause of shigellosis in developing world -S. sonnei -Most common cause of shigellosis in industrialized world -S. boydii -S. dysenteriae |
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EPIDEMIOLOGY
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-humans are the only carriers, transmitted via fecal-oral route
-very low inoculum (only 10-100 bacilli) -most cases in children ages 6-10 |
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MORPHOLOGY
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- Gram (-) rod
Significant outer membrane (drying) |
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PATHOGENESIS
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-attach an invade M cells in Peyer’s patches and cause membrane ruffling
-shiga exotoxin (S. dysenteriae) which disrupts protein synthesis - damage glomerular epithelial cells (hemolytic uremic syndrome) (compare entero _______ E. coli) |
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CLINICAL SYNDROMES
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-GI symptoms are caused by Shiga toxin (enterotoxic, neurotoxic, cytotoxic)
-Profuse, watery diarrhea -Fever -Tenesmus -abundant blood and pus in stool -NO VOMITING -Shigellosis: -Bactermia is RARE -Infection is generally self limited -5% of patients carry bacteria assymptomatically |
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TREATMENT
|
-same as enterobacteriaceae in general:
-proper hygiene -proper removal, isolation, disinfection of soiled linens and diapers -ABC are used to: -Shorted course of disease and control spread by reducing carriage in symptomatic patients -Resistance is likely (compare pseudomonas) -resistant to Stomach acid (low inoculum) (contrast Salmonella) |
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VIBRIOACAE, VIBRIO – family, genus, species
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-V. parahemolyticus
-V. vulnificus -V. Cholera (most known) -200 serotypes -EI tor biotype is most common in world today |
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MORPHOLOGY
|
-Gram (-) bacillus, comma shaped (compare legionella)
-Motile – single polar flagella -Most need salt for growth (“halophilic”) – NOT V. Cholera |
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VIRULENCE FACTORS (V. Cholera)
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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 |
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EPIDEMIOLOGY (V. Cholera)
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-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) |
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CHOLERA S/S
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-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 |
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CHOLERA LAB DIAGNOSIS
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-rarely seen in gram stained stool or wound specimens
-dark field / phase contrast microscopy – characteristic darting motility -direct ELIZA |
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CHOLERA TREATMENT, PREVENTION, CONTROL
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-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 |
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BACILLACEAE, BACILLUS – Family, genera
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- Gram (+) bacillus
- Endospore forming - 2 main species that cause disease in humans -B. anthracis – anthrax -B. cereus – gastroenteritis (contaminated “cereal,”rice) |
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B. ANTHRACIS
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-biological warfare
-Gram (+) bacillus -Clinical samples – single or paired – “jointed bamboo-rod” -Culture – long serpentine chains “medusa head” |
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VIRULENCE FACTORS
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a)Capsule
-anti-capsular antibodies are not protective b)Toxin -3 parts: -protective Ag – binding, antiphagocytotic -lethal factor – zinc metalloprotein, proinflammatory -edema factor – stimulate adenylyl cyclase fluid build up |
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EPIDEMIOLOGY
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-domestic herbivores – sheep, goats, cattle, horses
-3 routes of transmission -inoculation of the skin -most common – contacting infected animals – 20% mortality -inhalation of spores / wool – “woolsorter’s disease” – 95% mortality -ingestion of contaminated food – rare but deadly -endemic in developing countries -occupational disease and biological warfare in developed countries |
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CUTANEOUS ANTHRAX
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-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) |
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INHALATION ANTHRAX
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-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) |
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INGESTION ANTHRAX
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-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 |
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TREATMENT / PREVENTION
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difficult due to long lived spores –
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B. CEREUS
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-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) |
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VIRULENCE FACTORS
|
-heat stable enterotoxin - emesis. Found in contaminated, improperly refrigerated rice dishes
-heat labile enterotoxin - profuse watery diarrhea. Found in contaminated meat, vegetables, and sauces (compare enterotoxin of ETEC and V. cholera) -cerolysin - eye damage -phosopholipase C - eye damage -Necrotic toxin - eye damage |
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FOOD BORN DISEASE
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a)emetic disease
-NO FEVER -NO DIARRHEA b)diarrheal disease -nausea -bloody diarrhea -NO FEVER |
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PANOPTHALMITIS
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-post traumatic
-rapid (<48 hours) |
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TREATMENT AND PREVENTION
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a)Gastroenteritis
-no ABC (sickness due to toxin) -rapid consumption of food after eating??? -Refrigerate uneaten portions b)Panopthalmitis -early, aggressive ABC -multiple drug resistance |
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CAMPYLOBACTERACEAE (Family)
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-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) |
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EPIDEMIOLOGY
|
-number 1 bacterial cause of gastroenteritis and bacterial endocarditis in USA
-most common is C. jejuni -carried on birds, cats -also transmitted via raw milk and water -peak incidence in young adults (20-29 yo) |
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CAMPYLOBACTER JEJUNI GASTEROENTERITIS
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-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) |
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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? |
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TREATMENT AND PREVENTION
|
-Gastroenteritis
-Prevent with proper preparation and storage of food -Avoid raw milk -Proper water treatment -Guillan Barre syndrome -No treatment |
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HELICOBACTER PYLORI
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-Gram (-) bacillus – but gram stain is variable (spiral in fresh culture, coccoid in older culture)
-Motile – flagellated – “corkscrew motion” -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.) |
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EPIDEMIOLOGY
|
-found in gastric antrum and body of stomachs of humans, primates, pigs, cheetahs, dogs, cats, ferrets, mice, rats
-up to 45% in adults >50 yoa -only <20% of people testing positive for H. pylori get peptic ulcer disease |
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COLONIZATION FACTORS
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-survive acidity
-acid inhibitory protein -urease -flagella -mucinase – breaks down mucin layer in stomach -phospholipase -microaerophillic -survive in relatively anaerobic environment of stomach |
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VIRULENCE FACTORS
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-Pro-inflammatory – platelet aggravating factor - hyper-secretion of gastric acid
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DISEASES
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1.Type B (infective) gastritis (type A – is autoimmune due to NSAIDS)
-30-50% of people with gastritis have H. pylori but are most commonly asymptomatic -epigastric pain -foul smelling breath -lab diagnosis: -13C urea breath test -anti-H. pylori Abs (IgG) -gastroscopy with biopsy -CampyloLikeOrganism test (+) 2.Peptic ulcer disease -especially gastric ulcers -burning, gnawing upper GI pain 1-3 hours after meals - < night - >eating - >antacids - Lab diagnosis: - Endoscopy - Urea breath test - Serology (anti H. pylori Abs) 3. Gastric adenocarcinoma - class I carcinogen - S/Sx (similar to other cancers) -fatigue -weight loss -low grade fever -night pain -hemoccult (+) stools 4.Gastric mucosa-associated lymphoid type B cell lymphoma -rare -no evidence that eradicating H. pylori prevents progression of gastritis to carcinomas (something else must be going on) 5.Athersclerosis? |
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TREATMENT
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-triple therapy: proton pump inhibitor, clarithromycin, metronidazole, bismuth
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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 |
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C. PERFRINGENS
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-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 |
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PATHOGENICITY
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-spore formation – long term survival
-alpha toxin – most tissue damage – vascular permeability increases, lyses cells -heat kills enterotoxin |
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EPIDEMIOLOGY
|
-ubiquitous
-most commonly harmless saprophyte (live on dead tissue) -need devitalized tissue (anaerobic) -disease most common after trauma that causes ischemia – lowered pO2 and pH favors growth |
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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 |
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Lab DX
|
fast growth of culture on sheep’s blood agar
-nagler’s reaction on egg yolk agar -gram (+) rods in tissue specimens with no leukocytes |
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C. DIFFICILE
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-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 |
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VIRULENCE FACTORS
|
-Toxin A (enterotoxin) – hemorrhagic necrosis in pseudomembranous colitis (the key inflammatory players are IL-1, IL-6, and TNF alpha)
-Hyaluronidase – increase spread between tissues |
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DISEASES
|
-mild diarrhea to colitis to potentially life-threatening pseudomembranous colitis
-prolonged diarrhea (signs of dehydration) - pseudomembranous colitis is confirmed by biopsy – multiple, raised white / yellow exudative plaques adhering to colonic mucosa |
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lab dx
|
in vitro cytotoxicity assay in culture cells
-immuno assay (direct ELIZA) for C. difficile toxins A and B -sigmoidoscopy -fecal leukocytes |
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TREATMENT & PREVENTION
|
-maintain fluid / electrolyte balance
-avoid drugs / therapies that decrease intestinal motility -“watchful waiting” if mild -hand washing, environmental cleansing of play areas, beds, bathrooms -prescribe ABC w/ probiotics (but take away from each other, and taking probiotics with food, especially protein decreases stomach acidity which decreases likelihood of survival???) -for example: saccharomyces boulardii, lactobacillus spp. |
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C. TETANI “extreme tension”
|
-gram stain variable (compare helicobacter pylori)
-classic “tennis racket” -very sensitive to oxygen – obligate anaerobe -relatively inactive metabolically (contrast C. perfringens) |
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VIRULENCE FACTORS
|
-spores – survive adverse conditions (3 hours of boiling, 1 hour at 160° C of dry heat, 2 weeks in 5% phenol)
-tetanospasmin -heat labile neurotoxin – one of the three most potent toxins -responsible for spastic paralysis -two part toxin -irreversibly inhibits the release of GABA and glycine in post synaptic terminals in CNS (same mechanism as strycnin poisoning) |
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EPIDEMIOLOGY
|
-ubiquitous
-spores last for years -present in GIT of cows, horses, and some humans - low disease incidence in developed worlds due to immunizations, herd immunity, and urbanization - infant tetanus can be a problem in developing worlds contributing to > 50% of neonatal deaths |
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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 |
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OTHER FORMS OF TETANUS
|
-localized
-cephalic -neonatal – from improperly cleaned umbilical stump -firs sign: difficulty sucking 8-10 days after birth |
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Lab DX
|
-patient history
-clinical S/Sx -gram stain and culture not that important because only 30% of people with tetanus are culture (+) |
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TREATMENT & PREVENTION
|
-Tetanospasmin binds irreversibly and therefore can only treat symptoms until nerve terminal regenerate
-Passive immunization – binds free tetanospasmin -No natural immunity unlike many other diseases -Active immunization – tetanus toxoids: booster every 10 years |
|
C. BOTULINUM
|
-gram (+) bacillus “sausage shaped”
-produces one of the most potent exotoxins know to humans -ubiquitous – sediments of lakes and ponds |
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VIRULENCE FACTORS
|
-spore formation – one of the most resistant from heat (hours at boiling, 10 minutes at 120°C) and cold (down to -190°C)
-botulinum toxin -one of the most potent known neurotoxins -binds irreversibly to cholinergic neurons -inhibits acetylcholine release at peripheral presynaptic terminals and therefore causes a flacid paralysis (opposite of tetanospasmin) -botox for cosmetics, migraines, other disorders |
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FOOD BORNE BOTULISM – INTOXICATION
|
-inadequate sterilization of food – home canned foods, preserved fish
-2-72 hours incubation |
|
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 |
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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 |
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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%) |
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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 |
|
NEISSERIA
|
-gram (-) diplococci “coffee bean”
-transparent colonies on chocolate blood agar |
|
-N. meningitidis
-Normal colonizer of nasopharynx or cause disease |
-asymptomatically colonize nasopharynx or cause meningitis, meningococcemia or pneumonia
|
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PATHOGENESIS
|
cells
-Phagocytosis effective? -replicates in phagocytic vacuoles -capsule is also anti-phagocytic -LOS expressed? |
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EPIDEMIOLOGY
|
-most common cause of bacterial meningitis in infants through adolescence and in young adults
-epidemics -most common when a new virulent strain is introduced into an immunologically naïve population -transferred via close contact with respiratory droplets (et. Day cares, military barracks) -classmates in school, hospital employees not considered close enough contact to get disease - most common carriers are asymptomatic adults (nasopharyhgeal carriers) -disease is most common in dry, cold months |
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MENINGOCOCCEMIA
|
– mild disease
-persistent (few days to weeks): -arthritis -petechial skin rashes |
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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 gonococcu” -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 |
|
EPIDEMIOLOGY
|
-humans are the sole natural carriers of gonorrhea
-transmission: intimate sexual contact (most commonly in 15-24 year olds) -increased risk if female, with multiple sexual partners -women are most commonly asymptomatic carriers |
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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 |
|
LAB DIAGNOSIS
|
-clinical signs similar to chlamydia
-gram stain -sensitive and specific iff men with purulent urethritis -must confirm with culture -gram (-) diplococci on chocolate blood agar |
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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 |
|
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 |
|
EPIDEMIOLOGY
|
- can cause STD, most common to developing world
-causes chancroid (soft chancre) |
|
CHANCROID
|
H. ducreyi
Soft, purulent, painful ulcer (genitalia) MC in uncircumcised males tropical and sub-tropical (female – carrier) 5-7 day incubation 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 painless buboes Poor gram stain – dark field microscopy (spiral rods, thin tightly coiled), non-specific tests (VRDL, RPR), specific tests (FTA-Abs, TPHA) |
|
TREATMENT and PREVENTION
|
-ABC’s: ceftriaxone, erythromycin, cotrimazole
-Save sex practices |
|
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 |
|
EPIDEMIOLOGY
|
- can cause STD, most common to developing world
-causes chancroid (soft chancre) |
|
CHANCROID
|
H. ducreyi
Soft, purulent, painful ulcer (genitalia) MC in uncircumcised males tropical and sub-tropical (female – carrier) 5-7 day incubation 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 painless buboes Poor gram stain – dark field microscopy (spiral rods, thin tightly coiled), non-specific tests (VRDL, RPR), specific tests (FTA-Abs, TPHA) |
|
TREATMENT and PREVENTION
|
-ABC’s: ceftriaxone, erythromycin, cotrimazole
-Save sex practices |
|
HAEMOPHILUS INFLUENZAE
|
-non-encapsulated strains colonize both upper and lower respiratory tracts
-encapsulated strains (serotype b) can become systemic |
|
VIRULENCE FACTORS
|
a)Capsule
-determines serotype, virulence and tropism – invasive disease is most commonly due to H. influenzae type b (Hib infection) -antiphagocytotic -presence of anti-Hib capsule Abs determines severity of disease -transfer of maternal Abs is paramount to preventing disease b)pili c)LPS -damage respiratory, ciliated epithelium -responsible for meningitis d)IgA protease |
|
EPIDEMIOLOGY
|
-primarily a pediatric problem (don’t need to vaccinated after 5 years old, because by 6 should develop immunity)
- currently primarily a pediatric problem in developing world -also increase risk in elderly |
|
DISEASES
|
a)Meningitis
-same S/Sx as other bacterial meningitis – but more insidious onset and increased risk of neurological sequelae b)epiglottis -medical emergency -most common in boys 2-4 yoa -dysphagia, drooling, muffled voice (hot potato), minimal cough -severe dyspnea -“thumb sign” on lateral X-ray of neck c)cellulitis d)monoarticular arthritis e)Otitius media / sinusitis -3 most common causes are H. influenzae, S. pneumonia, Moraxella catarrhalis -(immune acquired pneumonia and otitis media in kids is most commonly caused by dairy and sugar) f)Pneumonia - might be 2° to influenzae virus damage to respiratory epithelium |
|
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 |
|
VIRULENCE FACTORS
|
1.pertussis toxin
-A/B5 structure -Increase adenylate cyclase - cAMP-respiratory secretions / mucus 2.adenylate cyclase toxin (cyclosin) -increase cAMP - protects bacteria against elimination in early infection (inhibits NK cell lysis, leukocyte chmotaxis, phagocytosis, and killing) 3.tracheal cytotoxin -part of peptidoglycan layer causing ciliostasis and then damage to epithelial cells -cough -increases IL-1 fever 4.dermonecrotic toxin 5.filamentous hemagglutin and other adesins -attachment to ciliated epithelial cells and PMN’s – intracellular survival protects against clearance by humoral immunity 6.LPS - two types (lipid A and lipid X) |
|
EPIDEMIOLOGY
|
-can only cause disease in humans
-most common in developing countries in children < 1yoa -spreads by infectious droplets -increased incidence in older individuals -no long term immunity |
|
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 |
|
LAB DX
|
-Bacteria are best isolated using nasopharyngela aspirates during catarrhal stage
-Microscopy: fluoresceine -Culture: difficult humidity, 35°C, 7 days, specialized agar – only 50% of infective people are culture positive -PCR -Lymphocytosis - >18,000 WBC w/ 70-80% lymphocytes |
|
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 effect”) |
|
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 |
|
LAB DX
|
-no gram stain, use silver and fluorescent stains
-non-specific tests: -Venereal Disease Research Lab, Rapid Plasma Reagent (both look for lipids) -Indicated current active disease -specific tests -Fluorescent Trepanemal Antigen-Abs and TPHA -Indicates past infection |
|
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 |
|
PATHOGENESIS
|
-inhaled into terminal airways and phagocytosed by alveolar macrophages
-the buggers evade humoral immunity because they grow intracellularly -spreads to other tissues - no known mycobacterial toxin or enzyme associated with tissue destruction which is primarily due to host response - form tubercles (the body trying to protect itself) caseous granulomas -Ghon complex – initial lung lesion and locally enlarged lymph nodes |
|
DISEASE
|
-“TB is the master impersonator”
-Primary infection: -insidious onset: malaise, listelessness, night sweats, low grade fever, unexplained weight loss and progressive fatigue -Chest X-ray shows cavitations -Secondary TB (reactivation): -Only 5-10% risk that active TB will develop at any time after exposure -Hematogenous spread anywhere -Milliary (seed like) TB w/ no pulmonary signs |
|
LAB DIAGNOSIS
|
- sputum sample: acid fast bacillus w/ fastidious growth requirements, PCR
- skin test (mantoux test): delayed hypersensitivity (T cell mediated) measure induration / erythema |
|
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 |
|
VIRULENCE FACTORS
|
-antiphagocytotic capsule
-preference for lower temperatures -intracellular survival -limits infection to skin and nasopharynx -schwann cells |
|
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 faces”) ->5 skin lesions |
|
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 |
|
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 |
|
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 |
|
MORPHOLOGY
|
-can be either:
-monomorphic: -Cryptococcus neoformans -dimorphic: -saprobic phase -in envirnment -parasitic phase – thermal dimorphism -in human infection |
|
HISTOPLASMA CAPSULATUM
|
-saprobic phase
-in N2 rich soil -parasitic phase – thermal dimorphism -in macrophages of Reticular Endothelial System / Mononuclear Phagocytic System |
|
EPIDEMIOLOGY
|
-found in “histo” belt
-grows in soils rich in N2 – agricultural belt uses much N2 as fertilizer -bird (starling / chicken) and bat excrement -epidemics from: -urbanerenewal -campsites -demolishing chicken coops -spelunking -researchers disturbing an environment rich in spores |
|
PATHOGENESIS
|
-inhale ->macrophages phagocytose -> replicated in macrophages -> carried by lymphatics to rest of body
|
|
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 |
|
LAB DIAGNOSIS
|
-microscopy: biopsy / histological exam – 10% KOH prep w/ silver or giemsa stain
-serological: skin test – too many false (+) -cultures: selective agar – slowly growing (1-2 weeks) and spores are infections -DNA probes -Direct ELISA |
|
BLASTOMYCES DERMATIDES
|
related to H. capsulatum
|
|
Morphology
|
related to H. capsulatum
|
|
epidemiology
|
endemic areas overlap those of histoplasmosis
-can cause disease similar to humans in dogs and horses and other animals -unknown reservoir (unlike H. capsulatum it is rarely cultured from soil) |
|
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 |
|
LAB DIAGNOSIS
|
-skin test and serology: too many false (+)
-microscopy: biopsy / histology of KOH prepped tissue sample -culture: on selective sabourand agar |
|
COCCIDIODES IMMITIS
|
-dimorphic
-37°C, tissue, mulitnucleated spherule “sporangia” -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
|
-skin test antigens – 2-4 weeks after sx
-coccidiodin – cell free culture of mycelium growth -spherulin – cell free culture of spherule phase -complement fixation -CXR – “egg shell lesions” -Tissue biopsy – spherules -Culture: CAUTION: infectious -> leading to lab acquired infections |
|
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 |
|
LAB DIAGNOSIS
|
-tzanck smear – synctia (multinucleated giant cells from fusion of neighboring cells) – (HSV, VZV, HIV)
-cowdry type A – inclusion bodies – histological changes caused by viral components or virus-induced changes in cell structure (HSV, VZV) -characteristic CypoPathological Effect’s – on specific cell lines |
|
TREATMENT
|
-allopathic – anti virals
-naturopathic – diet, tea tree oil, geranium oil |
|
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 |
|
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 |
|
EPIDEMIOLOGY
|
-very contagious from 48 hours before symptoms until all lesions are completely dry
-peak occurrence of chicken pox is 5-10 yoa - peak occurrence of shingles > 65 yoa - active herpes zoster can cause chicken pox in susceptible child or adult but will not cause shingles |
|
PATHOGENESIS
|
- 1° infection – 2-4 days after inhalation lymphatics
- 2° viremia – thoracic area, vesiculopapular rah - VZV becomes latent in DRG or cranial root ganglia -> reactivated in older adults and immunocompromised >dermatome ->shingles |
|
CHICKEN POX
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-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 |
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CHICKEN POX COMPLICATIONS
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° 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 |
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HERPES ZOSTER – shingles
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-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 |
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SHINGLES COMPLICATIONS
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-herpes zoster opthalmicus – CN V, III
-ramsay hunt syndrome (herpes zoster oticus) – painful lesions along CN VIII (severe otalgia, hearing loss, vertigo), CN V |
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DIAGNOSIS
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- 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 |
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VZV TX and CONTROL
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relatively mild disease that gives life-long immunity
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