Showing posts with label Infectious disease. Show all posts
Showing posts with label Infectious disease. Show all posts

13 June 2013

Nosocomial Infection - An infection acquired after hospitalization



Nosocomial Infection - An infection acquired after hospitalization

Nosocomial Antibiotic Resistant Organisms?
Pierre Magal etal
http://www.ncsu.edu

Mathematical Modelling and Challenges in the Development of Drug Resistance
Mary Ann Horn
http://math.la.asu.edu

Nosocomial Infection Control
Travis Reineke Fischer, Vijay Ramnath
http://www.hsi.gatech.edu

Surgical Site Infection: New Solutions to a Continuing Problem
R. Lawrence Reed
http://www.smbs.buffalo.edu

Surgical Infection
John Pender, MD
http://www.ecu.edu/

Nosocomial Antibiotic Resistant Organisms
http://www.nd.gov

Preventing Surgical Site Infections (SSIs): What the Direct Caregiver Should Know
Ann Bailey, RNC, BSN, CIC, Joanne Dixon, RN, MN, CIC
http://www.austincc.edu

Preventing Central Line Associated Bloodstream Infections (CLABSIs) - What Clinical Staff Should Know
Ann Bailey RNC-NIC, BSN, MBA, CIC, Joanne Dixon MN, RN, CIC, Gwen Irwin, RN, CRNI, Judy Smith, RN, BSN, CRNI
http://www.austincc.edu

Nosocomial Infections
Mark M. Huycke, M.D.
http://hippocrates.ouhsc.edu

Epidemiology And Nosocomial Infections
http://www-personal.umich.edu

Infection Control, Vital Signs, Oxygen & Medical Emergencies
http://www.elcamino.edu

Infection Control Nosocomial Infection
http://faculty.mdc.edu

Device Related Nosocomial Infection In ICU
http://www.pitt.edu

Prevention & Control Of Nosocomial Infections
Dr. A K.AVASARALA  MBBS, M.D.
http://www.pitt.edu/Part-1
http://www.pitt.edu/Part-2

Promoting Asepsis and  Infection Control
Teresa V.  Hurley, MSN, RN
http://faculty.msmc.edu

Asepsis and Infection ControlProfessor Susan Blakey, RN, MS
http://faculty.mercer.edu

Drugs Used to Treat Infections
http://home.apu.edu

Infection Control
http://www.twcnet.edu

Prevention & Control Of Nosocomial Infections
http://www.morgancc.edu

Principles of Disease and Epidemiology
http://faculty.rcc.edu

Microbe-Human Interactions: Infection and Disease
http://faculty.tcc.edu

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20 August 2012

Babesiosis



Parasitic Diseases Human Pathogenic Protozoans
http://iws.collin.edu

Ticks
Paul R Earl
http://www.pitt.edu

Babesia microti
Hannah Wilder & Nicole Johnson
http://course1.winona.edu

Zoonotic Parasites
http://peer.tamu.edu

Microbial Diseases of the Cardiovascular and Lymphatic Systems
Christine L. Case
http://www.dmacc.edu

Babesia microti
Marcus Williamson, Katie Hofkes, Kayla Jenness
http://course1.winona.edu

Babesia microti
Jessica Grams & Jennifer Wimpfheimer
http://course1.winona.edu

Differentiating Babesia from Malaria
Devak Desai
http://www.georgiahealth.edu

Piroplasms: Babesia & Theileria
http://www.striepen.uga.edu

Case Conference
Jason L. Sanchez, MD
http://www.tropical.umn.edu

Borrelia and Babesia in wild vertebrates, ticks, and humans in Florida
Kerry L. Clark, M.P.H., Ph.D.
http://conference.ifas.ufl.edu

Parasite is new concern for U.S. blood supply
Megan Walsh, Marie McCullough
http://alpha.lasalle.edu

The wildfire fighter with arthritis and fatigue
David P. Fitzgerald, MD
http://www.med.unc.edu


743 Published articles on Babesiosis

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26 June 2012

Onchocerciasis / River Blindness Lecture notes and 707 free access articles



Onchocerciasis also known as river blindness and Robles' disease, is a parasitic disease caused by infection by Onchocerca volvulus, a nematode. Onchocerciasis is the world's second-leading infectious cause of blindness.

River Blindness/ Onchocerciasis
Lawrence O. Gostin
http://www.pitt.edu/

Vector control
http://www.striepen.uga.edu/

CHALLENGING HEALTH PROBLEMS -WESTERN SUDAN
SULAIMAN, S. M.
http://www.pitt.edu

Blindness
Ines Serrano MD, Evan Waxman MD PHD
http://www.pitt.edu/

Ophthalmic Epidemiology
Michael B. Gorin, M.D. Ph.D.
http://www.pitt.edu/

Tropical Ophthalmology
Dr. Steve Waller
http://www.pitt.edu/
http://www.pitt.edu/

onchocerciasis
http://www.striepen.uga.edu/

River Blindness
http://courses.bio.unc.edu/

A Brief overview of Vector-Borne IIlness
Jill Gallin
http://www.columbia.edu/

Black-Flies, Biting Midges and Sandflies
http://www.uwyo.edu/

DNA barcoding for disease vectors
Daniel Adjei Boakye
http://barcoding.si.edu/

Lymphatic Filariasis / Elephantiasis Loiasis Onchocerciasis (river blindness)
Wafa Menawi
http://elearning.najah.edu/

Climate Change and Vector-Borne Disease
Durland Fish, Ph.D.
http://publichealth.yale.edu/

Use of GIS for Decision Making in the Onchocerciasis Control Program in West Africa
Alexander Coles
http://www.payson.tulane.edu/

Towards an ontology of vector-borne diseases
http://ontology.buffalo.edu/

The World of Parasites: A brief overview of the gruesome lives of parasites
Maya Merritt and Mindy Johnson
http://cipm.ncsu.edu

Neglected Tropical Diseases
Amy Kapczynski
http://gspp.berkeley.edu/

707 Published scholarly articles free access

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06 April 2012

H1N1 ppt and 100 Free full text articles



Parents’  Perceptions of H1N1  Risk Predict Child Vaccinations
Susan T. Heinze,  Ayala Y. Gorodzinsky, Jessica G. Drew,  & W. Hobart Davies
University of Wisconsin-Milwaukee
H1N1.ppt

H1N1  monovalent vaccine and miscarriage
Jonathan  L. Temte, MD/PhD
VaccineSafety.ppt

Influenza The Ultimate Emerging Infectious Disease
Influenza The Ultimate Emerging Infectious Disease.ppt

Influenza  Update for Wisconsin  Laboratories
Pete  Shult, PhD.
Influenza  Update.ppt

Swine Influenza
Swine Influenza.ppt

Viruses,  Viroids, and Prions
by Christine  L. Case
Viruses,  Viroids, and Prions.ppt

Viral Pneumonia
Cheryl  Pirozzi, MD
http://medicine.utah.edu/internalmedicine/Pulmonary/fellowship/presentations/2011/Viral_Pneumonia_cpirozzi.ppt

Replication  of Negative-Sense RNA Viruses (Mutipartite)
RNA Viruses.ppt
H1N1 100 Free full text articles

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23 March 2012

Zoonotic Diseases



Zoonotic Diseases: Any disease or infection that is naturally transmissible from vertebrate animals to humans and vice-versa is classified as a zoonosis.

Zoonosis
http://pathmicro.med.sc.edu/.ppt

Safety Concerns with Animals: - Zoonoses
Stephanie Matthews, Sarah Monzel
Guides/Zoonoses-Monzel.ppt

Avian influenza: Zoonosis
Vicente C. Manalo, Jr., DVM, Maria Fidelis Manalo, MD,
Avian influenza: Zoonosis.ppt

Principles of Communicable Diseases Epidemiology
Communicable Diseases.ppt

Mosquito-borne Zoonotic Diseases
Anthony A Marfin, MD, MPH, MA
Mosquito-borne Zoonotic Diseases.ppt

Introduction to Foreign Animal Disease (FAD’s) and Zoonosis
R.B. Baker, DVM, MS
Foreign Animal Disease  Zoonosis.ppt

Zoonotic  Diseases of Avian Origin
Zoonotic  Diseases of Avian Origin Zoonotic.ppt

Wildlife Diseases
Wildlife Diseases.ppt

Zoonosis
http://pathmicro.med.sc.edu/Zoonosis.ppt

Zoonotic Diseases
Dr. Paul Bartlett, MPH., DVM., Ph.D
http://www.pitt.edu/Zoonotic Diseases.ppt

Occupational Health and Animal Use
Gary L.White, D.V.M., M.M.S.
Occupational Health and Animal Use .ppt

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04 March 2012

Cryptosporidium Ppt




Cryptosporidium enteritis is an infection of the small intestine with the parasite Cryptosporidium that causes diarrhea.
Cryptosporidium parvum causes the disease Cryptosporidiosis
Cryptosporidium.ppt
Cryptosporidium  parvum
Melissa  Lamb
Parvum-Lamb.ppt

Waterborne Cryptosporidiosis Transmission Model
Elizabeth Casman, Mitch Small, Baruch Fischhoff, Claire Palmgren and Felicia Wu
http://hdgc.epp.cmu.edu/meeting99/casman-crypto.ppt

Cryptosporidiosis: You Are At Risk
By: Sarah Ruth  Davis
CryptoPresentationSRD.ppt

Protozoan Diseases
Protozoa.ppt

Water-borne  Diseases
By Yenisel Cruz
Water-borne  Diseases.ppt

Read more...

14 February 2012

Tetanus neonatorum Ppts and latest published articles




Tetanus neonatorum: etanus affecting newborns, usually due to infection of the severed umbilical cord. Highly fatal disease caused by the bacillus Clostridium tetani, characterized by muscle spasms and convulsions.

Tetanus
by DR.I. Selvaraj I.R.M.S
24011-25001/24031.ppt

Tetanus neonatorum
Tetanus_neonatorum.ppt

Diphtheria
Diphtheria.ppt

Tetanus
by Dr.Vemuri  Chaitanya
Presentations/tetanus.ppt

Brucellosis,  Tetanus & Plague 
By Dr.  Riaz Ahmed
Tetanus.ppt

Tetanus
By Chandana  Krishna
Tetanus-chandana.ppt

Latest 50 Published articles

  1. Miasma or contagion. Neonatal tetanus (tetanus neonatorum) at the Westman Islands and dr Peter Anton Schleisner's effort to control it.
  2. Tetanus neonatorum in Sierra Leone.
  3. Tetanus neonatorum. Historical intent of its prevention in Latin America.
  4. Tetanus neonatorum: evaluation of 4 therapeutic regimens.
  5. A case of maple syrup urine disease misdiagnosed as tetanus neonatorum on admission.
  6. A new method of grading tetanus neonatorum.
  7. A review of 43 cases of tetanus neonatorum.
  8. A study of tetanus neonatorum: different regimens of treatment.
  9. Birth care practice and tetanus neonatorum: a hospital-bases study in Mosul.
  10. Clinical study of tetanus neonatorum.
  11. Control of tetanus neonatorum in a rural area.
  12. Double-blind trial of intramuscular and intramuscular plus intrathecal human tetanus immunoglobulin and intramuscular equine tetanus antitoxin in the treatment of tetanus neonatorum.
  13. Evaluating tetanus neonatorum as a child survival risk in rural Egypt in the absence of reliable cause-of-death registration.
  14. Evaluation of intrathecal human tetanus immunoglobulins in tetanus neonatorum.
  15. Failure of intrathecal tetanus antitoxin in the treatment of tetanus neonatorum.
  16. Fractures of the acromion in tetanus neonatorum corrected.
  17. Impact of alternate immunisation strategies on tetanus neonatorum in India.
  18. Impact of universal immunization programme on the incidence of tetanus neonatorum.
  19. Intermittent positive pressure respiration in tetanus neonatorum. 1960.
  20. Intrathecal anti-tetanus serum in management of tetanus neonatorum.
  21. Management of tetanus neonatorum in a respiratory unit.
  22. Modern management of tetanus neonatorum.
  23. Mortality from tetanus neonatorum in Punjab (Pakistan).
  24. Permanent tetraplegia as a consequence of tetanus neonatorum. Evidence for widespread lower motor neuron damage.
  25. Prevention of tetanus neonatorum.
  26. Pyridoxine in tetanus neonatorum.
  27. Pyridoxine in the treatment of tetanus neonatorum.
  28. Pyridoxine therapy in tetanus neonatorum.
  29. Role of intrathecal tetanus antitoxin (equine) in tetanus neonatorum.
  30. Semiprone position and continuous intragastric drip in conservative management of tetanus neonatorum.
  31. Single dose tetanus toxoid--a review of trials in India with special reference to control of tetanus neonatorum.
  32. Some aspects of tetanus neonatorum in the Pretoria area.
  33. Study of tetanus neonatorum in Tanta Fever Hospital, 1988-1989.
  34. Tetanus nascentium, neonatorum, or infantum.
  35. Tetanus neonatorum (a preliminary report of assessment of different therapeutic regimens).
  36. Tetanus neonatorum as seen in Kalawati Saran Children's Hospital, New Delhi in the year 1965 and a decade later.
  37. Tetanus neonatorum in babies delivered by traditional birth attendants in Medan, Indonesia.
  38. Tetanus neonatorum.
  39. Tetanus neonatorum.
  40. Tetanus neonatorum. (A preliminary report on the assessment of different therapeutic regimens).
  41. Tetanus neonatorum: A continuing problem.
  42. Tetanus neonatorum: clinico-epidemiological profile.
  43. Tetanus neonatorum--experience with intrathecal serotherapy at Muhimbili Medical Centre, Dar es Salaam, Tanzania.
  44. Tetanus neonatorum--experience with intrathecal serotherapy at Muhimbili Medical Centre Dar es Salaam.
  45. Tetanus neonatorum--its epidemiology and management.
  46. The influence of pyridoxin in the treatment of tetanus neonatorum.
  47. Traditional birth attendants in an endemic area of tetanus neonatorum in Thailand: pitfalls in the control program.
  48. Treatment of tetanus neonatorum in a rural setting.
  49. Treatment of tetanus neonatorum--with special reference to hyperimmune blood transfusion.
  50. Trial of pyridoxine therapy for tetanus neonatorum.

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29 April 2010

Bacteria Pathogenicity Ability to Cause Infection



Bacteria Pathogenicity Ability to Cause Infection

Infectious Diseases
* Encounter-bug meets host (reservoir)
* Bug adheres to host
* Entry-bug enters host
* Multiplication- bug multiplies in host
* Damage to host
* Outcome- bug or host wins or
* Coexist- chronic infection

Reservoir
* Exposure to microbe
Virulence Factors
Adherence
* Prevent infection
* Influenza changes adhesions over time
* Neisseria gonorrhoeae -variety of adhesions

Portals of Entry
* Mucous membranes
* Conjunctiva
* Skin
* Bugs have preferred portal
* C. tetani spores in soil --- anaerobic wound

Inoculum

* Number of microbes-dose
* Greater dose, more chance infection will occur
* ID50 or LD50 expresses virulence

Invasins
* Adherence of microbe to surface
* Activates factors that let microbe in-penetration
* Microbes produce invasins (proteins)
* Endocytosis
* Requires multiplication
* Compete with normal flora for space & nutrients
* Overcome local host defenses
* Avoid IgA

Multiplication
* Need Fe to multiply
Avoid Phagocytosis
* Components of cell wall –virulence
Surviving Within Phagocyte

Tuberculosis
* Ancient disease
* 1/3 of world population infected
* 8 million develop active TB each year
* 2 million die each year
* AIDs increases activation of latent TB
* Dependent upon virulence of strain & host resistance
* Produces cell mediated immunity which prevents active disease in many people
* Multi drug resistance has developed

S & S of Pulmonary TB
* Chronic disease
* Progressive weight loss
* Night sweats
* Chronic cough
* Hemoptysis
Mycobacterium tuberculosis
* Acid fast bacillus (AFB)
* Resistant to drying
* Aerobic, slow growth
* Airborne transmission
* Inhale airborne droplets
* Ingested by alveolar macrophages
* Multiply in macrophages even with ongoing immune response

TB Response
* Host immune response-delayed type hypersensitivity reaction
* Tissue damage DT Inflammatory response
TB Conversion
* TST skin reaction is positive
* Occurs within 24 – 48 hours after exposure to TB antigens
* Purified protein derivative of bacillus
* Cell mediated immunity
* Sensitized T cells react with proteins
QuantiferonGold
* Blood test
* Detects interferon gamma

How to Confirm Diagnosis
* Sputum cultures for AFB smear & culture
* Chest xray
Pathogenesis
* LTBI (latent TB infection)
Active Disease

* Low resistance

TB Outcomes
* Primary infection- positive skin test
* 10% progressive primary infection-not controlled
Secondary or Reactivation Infection
* Reinfection-2nd exposure or
* Bacteria escape immune system-reactivation
* Activated macrophages release cytokines
* Delayed hypersensitivity reaction

Prevention of Transmission
* Negative pressure rooms
* Respirator masks-fit tested
* Admit staff aware of symptoms of TB
* Yearly TST of staff
* Conversions treated with 6-9 months of INH

Treatment
* INH for LTBI or TB conversion
* TB disease-active TB
* 9- 12 months of treatment
Resistant TB
* MDR TB
* XDR TB
* DT improper treatment

BCG
* Live culture of M. bovis
Latent vs Active
* Latent TB
* Active TB
Leprosy
* Hanson’s disease- discovered in 1873
* Seen in tropics and underserved countries
* U.S.-150 new cases per year
* Infection of nervous system
* Infects the peripheral nerves within skin
* 2 forms of disease dependent upon immune response

M. leprae
* Tuberculoid form
Lepromatous Form
* Weak immune response & microbe spreads
* Skin & nerve cells infected
* Shed large #s in nasal secretions and oozing sores-more infectious
Invasion via Enzymes
Kinases
Enzymes
Invasion via Toxins
Exotoxins
A-B Toxins
Superantigens
Naming of Exotoxins
Endotoxin
S & S
Shock
Staphylococci
S. aureus
Successful Pathogen
Biofilm
Capsule
Skin Infections
Invasion via Toxins
Toxic shock syndrome
S. aureus Intoxication
Treatment
CA-MRSA
Outbreaks in Community
PVL Gene
Preventing Transmission
Clostridium botulinum
Neurotoxin
Botulism-Foodborne Disease
Toxin
Clostridium tetani
Neurotoxin
Lockjaw
Clostridium difficile
Epidemiology
Range of Disease
Pathogenesis of CDI
New Issues
Treatment
Transmission
Environment

* Clean and disinfect surfaces in close proximity of the patient
* Patient care equipment.
* Use bleach for C. difficile
* Privacy drapes

Bacteria Pathogenicity Ability to Cause Infection.ppt

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11 April 2010

Infectious Diseases of the Respiratory System



Infectious Diseases of the Respiratory System

Infections of the Respiratory tract
* Most common entry point for infections
* Upper respiratory tract
* Lower respiratory tract


Protective Mechanisms
Normal flora: Commensal organisms
* Limited to the upper tract
* Mostly Gram positive or anaeorbic
* Microbial antagonist (competition)

Other Protective Mechanisms
* Nasal hair, nasal turbinates
* Mucus
* Involuntary responses (coughing)
* Secretory IgA
* Immune cells

Selected Bacterial Infections

Pharyngitis
Pneumonia - Streptococcus pneumoniae
Diphtheria - Corynebacterium diphtheriae
Tuberculosis - Mycobacterium tuberculosis
Whooping cough - Bordetella pertussis
Streptococcus pyogenes
Group A Strep
Strep Throat
Scarlet Fever
Bacterial Pneumonia
Streptococcus pneumoniae
Bacterial Pneumonia
Streptococcus pneumoniae
Diphtheria
* Transmitted by droplets or fomites
* Infects the upper respiratory tract
* Begins with severe sore throat, low-grade fever and swollen lymph nodes or with skin rash, 1-6 days after infection

Corynebacterium diphtheriae
* Aerobic Gram + bacillus
* Toxin inhibits protein synthesis of cells to which it binds
* Destroyed cells and WBC form "pseudomembrane" which blocks airways
Bordetella pertussis
Pertussis (Whooping Cough)
Mycobacterium tuberculosis
Tubercule formation
Tuberculosis
Multi-Drug Resistant
TB Skin Test
Virus infections
Fungal Infections
Respiratory Syncytial Virus
* Enveloped (membrane) RNA virus
* Spread by respiratory droplets
* Community outbreaks in late fall to spring
* Upper respiratory tract infection – epithelial cells
* May be fatal in infants
Influenza Virus
An enveloped RNA virus
Coccidioides immitis
Valley Fever is an Endemic Disease
Coccidioides immitis

Infectious Diseases of the Respiratory System.ppt

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Upper Respiratory Tract Infections



Upper Respiratory Tract Infections
By:Dr. Meenakshi Aggarwal MD
Emory Family Medicine

Definition

* Inflammation of the respiratory mucosa from the nose to the lower respiratory tree, not including the alveoli.

Objectives
* List the various categories of upper respiratory tract infections
* Obtain a pertinent history in a patient with a suspected URI.
* Perform a targeted and thorough physical examination to confirm the diagnosis of URI.
* Perform and interpret selected tests to diagnose URI
* Manage and treat uncomplicated URI’s.

Categories
* Acute Rhinosinusitis
* Acute Pharyngitis
* Acute Bronchitis

Differential Diagnosis
* Influenza
* Pneumonia
* Tuberculosis
* Asthma

Anatomy of Sinuses
Acute Rhinosinusitis (Viral)
* Common Symptoms: Nasal discharge, nasal congestion, facial pressure, cough, fever, muscle aches, joint pains, sore throat with hoarseness.
* Symptoms resolve in 10-14 days
* Common in fall, winter and spring.
* Treatment: Symptomatic

Acute Bacterial Sinusitis
* Causative agents are usually the normal inhabitants of the respiratory tract.
* Common agents:

Streptococcus pneumoniae
Nontypeable Haemophilus Influenzae

Moraxella Catarrhalis
Signs and Symptoms
* Feeling of fullness and pressure over the involved sinuses, nasal congestion and purulent nasal discharge.
* Other associated symptoms: Sore throat, malaise, low grade fever, headache, toothache, cough > 1 week duration.
* Symptoms may last for more than 10-14 days.

Diagnosis
* Based on clinical signs and symptoms
* Physical Exam: Palpate over the sinuses, look for structural abnormalities like DNS.
* X-ray sinuses: not usually needed but may show cloudiness and air fluid levels
* Limited coronal CT are more sensitive to inflammatory changes and bone destruction

Ethmoid Sinusitis
Coronal computed tomographic scan showing ethmoidal polyps. Ethmoid opacity is total as a result of nasal polyps, with a secondary fluid level in the left maxillary antrum.

Treatment
* About 2/3rd of patients will improve without treatment in 2 weeks.
* Antibiotics: Reserved for patients who have symptoms for more than 10 days or who experience worsening symptoms.
* OTC decongestant nasal sprays should be discouraged for use more than 5 days
* Supportive therapy: Humidification, analgesics, antihistaminics
a) Amoxicillin (500mg TID) OR
b) TMP/SMX ( one DS for 10 days).
c) Alternative antibiotics: High dose amoxi/clavunate, Flouroquinolones, macrolides

Antibiotics
Acute Pharyngitis
* Fewer than 25% of patients with sore throat have true pharyngitis.
* Primarily seen in 5-18 years old. Common in adult women.

Etiology
A) Viral: Most common.
Rhinovirus (most common).
Symptoms usually last for 3-5 days.

B) Bacterial: Group A beta hemolytic streptococcus (GABHS).
Early detection can prevent complications like acute rheumatic fever and post streptococcal GN.

Signs and Symptoms
* Absence of Cough
* Fever
* Sore throat
* Malaise
* Rhinorrhoea
* Classic triad of GABHS: High fever, tonsillar exhudates and ant. cervical lymphadenopathy.

NO COUGH
Diagnosis
* Physical Exam: Tonsillar exhudates, anterior cervical LAD
* Rapid strep: Throat swab. Sensitivity of 80% and specificity of 95%.

Throat Cultures: Not required usually. Needed only when suspicion is high and rapid strep is negative.

Exhudates
Management
A) Symptomatic: Saline gargles,

analgesics, cool-mist humidification and throat lozenges.

B) Antibiotics:
a) Benzathine Pn-G 1.2 million units IM x 1OR Pn V orally for 10 days
b) For Pn allergic pts:Erythromycin 500mg QID x 10 days OR Azithro 500 mg Qdaily x 3 days.

Acute Bronchitis
Inflammation of the bronchial respiratory mucosa leading to productive cough.
Acute Bronchitis
* Etiology: A)Viral
B) Bacterial (Bordetella pertussis, Mycoplasma pneumoniae, and Chlamydia pneumoniae)
* Diagnosis: Clinical
* S/S: Productive cough, rarely fever or tachypnea.

Treatment
* Symptomatic
* If cough persists for more than 10 days:

Azithro x 5 days OR
Clarithro x 7 days
Non specific URI’s

* Common Cold
* Etiology: Rhinovirus
Adenovirus
RSV
Parainfluenza
Enteroviruses
Diagnosis: Clinical
Treatment: Adequate fluid intake, rest, humidified air, and over-the-counter analgesics and antipyretics.

Influenza
* Etiology: Influenza A & B
* Symptoms: Fever, myalgias, headache, rhinitis, malaise, nonproductive cough, sore throat
* Diagnosis: Influenza A &B antigen testing
* Treatment: Supportive care, oseltamivir, amantidine

Upper Respiratory Tract Infections.ppt

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29 March 2010

Emerging Infections and Medical Procedures



Emerging Infections and Medical Procedures
By:Lennox K. Archibald, MD, PhD, FRCP
Hospital Epidemiologist, University of Florida

Parasitic Infections:
Clinical Manifestations, Diagnosis and Treatment

The Reality
* 1.3 billion persons infected with Ascaris (1: 4 persons on earth)
* 300 million with schistosomiasis
* 100 million new malaria cases/yr
* At UCLA, 38% of pediatric and dental clinic children harbored intestinal parasites

Infections Deaths

Parasites
* Organisms that cannot survive outside their host, AND they cause some harm to the host.
* Contrast with commensal organisms
* Incredibly complex organisms
* Consider the struggle for survival from the perspective of a parasite

Giardia
Giardiasis (G. lamblia)
* Should be suspected in prolonged diarrhea
* Contaminated water often implicated—outbreaks
* Campers who fail to sterilize mountain stream water
* Person-person in day care centers
* MSM
* Symptoms usually resolve spontaneously in 4-6 weeks
* Tests of choice
o Examination of concentrated stools for cysts (90% yield after 3 samples); usually no PMNs
o Stool ELISA, IF Antigen (up to 98% sensitive/90-100% specific)
o Consider aspiration of duodenal contents--trophozoites
* Treatment: Metronidazole for 5-7 days

Entamoeba histolytica
* One of 7 amoebae commonly found in humans
* Only one that causes significant disease
* Causes intestinal disease (diarrhea and dysentery) and extra-intestinal disease (liver primarily)
* In US, often seen in institutionalized patients, MSM, tourists returning from developing countries, patients with depressed cell mediated immunity
Cyst (wet mount)
* Diagnostic smear: trophozoites in liquid stools, cysts in formed stools
* IHA important in liver abscess
o Intestinal: 95% predictive of active infection
o Extra-intestinal: 100% predictive of active I infection

Amoebiasis: Clinical Manifestations
* Symptoms depend on degree of bowel invasion
o Superficial: watery diarrhea and nonspecific GI complaints
o Invasive: gradual onset (1-3 weeks) of abdominal pain, bloody diarrhea, tenesmus
* Fever is seen in minority of patients
* Can be mistaken for ulcerative colitis
* Steroids can dramatically worsen and precipitate toxic megacolon
* Amebic liver abscesses
o RUQ pain, pain referred to right shoulder
o High fever
o Hepatomegaly (50%)

Amoebic abscess—remember…
* Can occur in lung, brain, spleen
* That stool is merely a convenient vehicle passing by
* Amoebae live the bowel wall
* Direct observation preferable to mere examination of stool
* Trophozoites best seen in direct scrapings of ulcers
* Liquifaction of liver cells
* Do not contain pus
* Anchovy paste sauce
* Culture of contents usually sterile
* Liver affected
o 53%--right lobe
o 8%--left lobe

Amoebiasis (Entamoeba histolytica)
Treatment
* Most respond to metronidazole
* Open surgical drainage should be avoided, if at all possible

Cryptosporidium
Cryptosporidium parvum
* Causes secretory diarrhea: 10 liter/day
* Significant cause of death in HIV/AIDS
* Animal reservoirs
* Incubation period: 5-10 days
* Infants and younger children in day-care centers
* Unfiltered or untreated drinking water
* Farming practices: lambing, calving, and muck-spreading
* Sexual practices that brings a person into oral contact with feces of an infected individual
* Nosocomial setting with other infected patients or health-care employees
* Veterinarians: contact with farm animals
* Travelers to areas with untreated water
* Living in densely populated urban areas
* Owners of infected household pets (rare)

Diagnosis and Treatment
* Best diagnosed by stool exam
* There is no known effective treatment-nitazoxamide shortens duration of diarrhea
o Infectious disease specialist - for consideration of antiparasitic and antiretroviral therapy
o Gastroenterologist - ERCP and sphincterotomy; endoscopy sometimes required for diagnosis
o General surgeon - suspected acalculous cholecystitis

Malaria
Falciparum vs. Vivax
* Location: Falciparum confined to tropics and subtropics; vivax more temperate
* Falciparum infects RBC of any age; others like reticulocytes; only 2% infected cells
* Falciparum infected RBCs stick to vascular endothelium causing capillary blockage; fewer schizonts in the periphery, heavy pigment deposition, cerebral and renal disease
* Vivax and Ovale may reinfect hepatocytes, leading to a persisting tissue phase, causing relapses
* Sickle cell trait protects against Falciparum
Malaria: Genetic susceptibility
* Two genetic traits associated with decreased susceptibility to malaria
o Absence of Duffy blood group antigen blocks invasion of Plasmodium vivax
+ Significant number of Africans
o Persons with sickle cell hemoglobin are resistant to P. falciparum
+ Sickle cell disease and trait

Malaria: Clinical manifestations
* Non-specific, flu-like illness
* Incubation
* Fever is the hallmark of malaria
* Fever occurs after the lysis of RBCs and release of merozoites
* Febrile paroxysms have 3 classic stages
* Other symptoms depend upon the strain of malaria
* P. vivax, ovale and malariae: few other sxs
* P. falciparum:
* Always suspect malaria in travelers from developing countries who present with:
o Influenza-like illness
o Jaundice
o Confusion or obtundation

Diagnosis
* Giemsa-stained blood smear
* P. falciparum:
* Others:
* Examine blood on 3-4 successive days
* Key of diagnosis is to identify P. falciparum
* New assays: o ELISA for antigen, immunoassay for LDH, PCR
* Anemia, elevated LDH, increased reticulocytes, thrombocytopenia
* Elevated unconjugated bilirubin without increases in hepatic enzymes
* Elevated serum creatinine, proteinuria, hemoglobinuria, hypoglycemia

Differences in strains
* P. falciparum
* P. vivax and ovale
* P. malariae

Early troph--ring
Mature troph
Schizont
Gametocyte
Treatment
* P. falciparum malaria can be fatal if not promptly diagnosed and treated
* Pts with no immunity against P. falciparum require hospitalization
o Pregnant women, young children, elderly
* Non- P. falciparum malaria rarely requires hospitalization
* Widespread drug resistance dictates regimen (www.cdc.gov/travel; CDC malaria hot line: 770-488-7788).
* Uncomplicated malaria
o Drug options
+ Chloroquine phosphate
+ Mefloquine
+ Quinine sulfate plus doxycycline
+ Atovaquone plus proguanil (AP)
+ Artemisin derivatives
* P. vivax, ovale, malariae, chloroquine-susceptible falciparum
+ Chloroquine
+ Primaquine

Prevention
* Chloroquine
* Mefloquine
* Doxycycline
* Atovaquone plus proguanil (AP)
* Screens, nets
* 30-35% DEET
* permethrin spray for clothing and nets

And don’t forget baggage malaria!
Leishmaniasis
* Tropical areas where phlebotomine sandfly is common:
o South America
o India
o Bangladesh
o Middle East
o East Africa
* Sandfly introduces flagellated promastigote into human ingested by macrophages develops into nonflagellated amastigote
* Intracellular parasite controlled by Th1-type CD8+ response
Leishmaniasis: Clinical Manifestations
* 3 forms: visceral, cutaneous, mucosal
* A single species can produce more than one syndrome, and each syndrome is caused by multiple different species
* Visceral (kala azar)
o Species most prevalent in different places
# L. donovani – India
# L. infantum – Mid East
# L. chagasi – Latin America
# L. amazonensis -- Brazil
* Cutaneous
* Mucosal
Visceral Leishmaniasis
* Dissemination of amastigotes throughout the reticulendothelial system of the body
* Opportunistic infection in AIDS patients
* Ineffective humeral response
Hepatosplenomegaly
Splenic aspirate
* Most satisfactory method
* Spleen must be at least 3cm below LCM
* PT not more than 5 secs longer than controls
* Platelets >40,000
* 21 gauge needle
* Aspirate stained with Giemsa

Leishmaniasis: treatment
* Only drug approved in US is Amphotericin B
* Outside US: pentavalent antimony (sodium stibogluconate)
* Treatment of cutaneous disease depends on anatomic location
* Many spontaneously heal and do not require treatment
* If no mucosal disease and areas of no cosmetic concern:
o 15% paromomycin or 12% methylbenzethonium chloride
* Mucosal, progressive lesions or cosmetically sensitive locations:
o Pentavalent antimony or ketoconazole

Remember..
* The factors determining the form of leishmaniasis:
o Leishmanial species
o Geographic location
o Immune response of the host

Toxoplasmosis
Toxoplasma gondii
* Worldwide distribution
* Human infection
* Prevalence of latent infection in US about 10%; France about 75%
o Generally higher in less-developed world
Transmission
* Eating oocysts excreted by cats harboring sexual stages of parasite
* Outbreaks traced to inadequately cooked meat of herbivores (raw beef)
* Mutton
Toxoplasma gondii: life cycle
Immunocompetent hosts
* Latent infection (persistence of cysts) is generally asymptomatic
* Cervical lymphadenopathy (10-20%)
* Mono-like presentation (<1% of all mono-like illnesses) * Chorioretinitis * Very rare: myocarditis, myositis Toxoplasma gondii: Immunocompromised hosts * Often life-threatening * Almost always reactivation of latent infection * AIDS o Encephalitis most common manifestation o Usually subacute onset/focal (if CD4< 200) o Mental status changes, seizures, weakness, cranial nerve abnormalities, cerebellar signs, o Can present as acute hemiparesis/language deficit o Usually multiple ring-enhancing lesions on CT/MRI * Pneumonitis * Chorioretinitis Toxoplasma gondii: Clinical manifestations * Immunocompromised hosts o Non-AIDS (transplants, hematologic malignancies) * Congenital * Acute infection asymptomatic in mother * Clinical manifestations range: no sequelae to sequelae that develop at various times after birth o Chorioretinitis o Strabismus o Blindness o Epilepsy, mental retardation, pneumonitis, microcephaly, hydrocephalus, spontaneous abortion, stillbirth Toxoplasma gondii: diagnosis * Clinical suspicion crucial * Serology is primary method of diagnosis o IgM, IgG * Histopathology o Tachyzoites in tissue sections or body fluid (difficult to stain) o Multiple cysts near necrotic, inflammatory lesions Toxoplasma gondii: Treatment * Immunocompetent adults are usually not treated unless visceral disease is overt or symptoms are severe and persistent * Immunodeficient patients * Congenital: Ascaris lubricoides Ascaris lumbricoides * In GI tract, few symptoms in light infectionst. * Pulmonary: symptoms due to migration Effects of Adult Ascaris Worms * Depends on worm load * Effects * Toxic and Metabolic Ascaris lumbricoides Diagnosis * Characteristic eggs on direct smear examination * If treating mixed infections, treat Ascaris first o Mebendazole 100 mg bid x 3 days o Pyrantel 10 mg/kg single dose * Control: o Periodic mass treatment of children, health education, environmental sanitation Enterobius (Pinworm) * 18 million infections in U.S. * Incidence higher in whites * Preschool and elementary school most often * Mostly asymptomatic * Nocturnal anal pruritis cardinal feature due to migration and eggs * May have insomnia, possible emotional symptoms * DS-eggs or adults on perineum {scotch tape} * Mebendazole 100 mg. Repeat in 2 weeks. Pyrantel pamoate 11 mg/kg; repeat 2 weeks Strongyloides Strongyloides: Crucial Aspects of Life Cycle * Infection acquired through penetration of intact skin * Infection may persist for many years via autoinfection * In immunocompromised patients, there is risk of dissemination or hyperinfection o Hyperinfection syndrome Disseminated Strongyloidiasis * High mortality 75% * Penetration of gut wall by infective larvae * Gut organisms carried on the surface of larvae results in polymicrobial sepsis, meningitis * Larvae disseminate into all parts of body: CNS, lungs, bladder, peritoneum Summary—Clinical Findings * Defective cell-meditated immunity: steroids, burns, lymphomas, AIDS (?) * Gl symptoms in about two-thirds: o Abdominal pain o Bloating o Diarrhea o Constipation * Wheezing, SOB, hemoptysis Summary—Clinical Findings * Skin rash or pruritis in ~ one-third * Eosinophilia 60-95% * Less if on steroids Hookworm * Hookworm responsible for development of USPHS * Caused by two different species (North American and Old World) * Very similar to strongyloides in life cycle * Attaches to duodenum, feeds on blood * Elaborates anticoagulant, attaches and reattaches many times * Loss of around 0.1 ml/d of blood per worm Cutaneous larva migrans (creeping eruption) * Caused by filariform larvae of dog or cat hookworm (Ancylostoma braziliense or Ancylostoma duodenale * Common in Southeast U.S. * Red papule at entry with serpiginous tunnel * Intense pruritis * Self limiting condition * Diagnosis clinical * Topical or oral thiabendazole 25 mg/kg bid for 3-5 days * May use ethyl chloride topically * More common in children o Larvae penetrate skin and cause tingling followed by intense itching. * Eggs shed from dog and cat bowels develop into infectious larvae outside the body in places protected from desiccation and extremes of temperature * Shady, sandy areas under houses, at beach, etc. Usually not associated with systemic symptoms * Diagnosis and treatment * Skin lesions are readily recognized * Usually diagnosed clinically * Generally do not require biopsy # Reveal eosinophilia inflammatory infiltrate # Migrating parasite is generally not seen * Stool smear will reveal eggs Visceral Larva Migrans * Infection with dog or cat round worms * Toxocara canis; Toxocara catis * Underdiagnosed based on seroprevalence surveys * Heavy infections associated with fever, cough, nausea, vomiting, hepatomegaly, and eosinophilia * Uncommon in adults * Ocular type more common in adults * Diagnosis-ELISA * Thiabendazole: 25 mg/kg bid X 5 days Echinococcosis Hydatid Disease Echinococcosis * Clinical manifestations: o Most patients are asymptomatic + Dx’d incidentally on an imaging study o Sxs generally develop when the hydatid cyst reaches 8-10 cm (often over decades) + Compress vital structures + Erode into biliary tract or bronchus o Cysts can become superinfected o Leakage or rupture can result in anaphylactic reaction  fever, hypotension Echinococcosis * Diagnosis: o US, CT or MRI + Characteristic hydatid cyst with septated daughter cysts + May see head of the tapeworm o ELISA + Highly sensitive for liver cysts, less so for other organs Echinococcosis (Treatment) * Surgical resection of cyst * To reduce risk of spread: o Aspirate cyst o Instill hypertonic saline, iodophor, 95% ethanol to kill germinal layer and daughter cysts o No cidal agents in cases with biliary communication  risk of sclerosing cholangitis * Percutaneous aspiration-injection-reaspiration (PAIR) * Albendazole before and after surgery or PAIR Schistosomiasis Schistosomiasis: Epidemiology and life cycle Schistosomiasis: Clinical manifestations Schistosomiasis: Diagnosis and treatment * Detection of characteristic eggs in stool, urine or tissue biopsy is diagnostic o Urine is best between 12N and 2Pm, passed through 10 µm filter to concentrate eggs * Antibody tests are available, but limited by sensitivity, specificity * Praziquantel is the drug of choice S. mansoni Stool S. haematobium Urine S. japonicum African trypanosomiasis Trypanosoma brucei gambiense Blood smear Tsetse fly Treatment * Suramin * Melasoprol American trypanosomiasis Blood smear Reduviid bug (assassin bug) Chagas disease: Clinical manifestations Chagas disease: Diagnosis and treatment * Acute disease is diagnosed by seeing trypomastigotes on peripheral blood smear * Chronic disease is diagnosed by ELISA detecting IgG antibody to T. cruzi * Both acute and chronic disease can be treated with nifurtimox or benznidazole * Treatment slows the progression of heart disease Chagas Disease * Public health implications in the US * Chronic o Cardiomyopathy o Megaesophagus o Magacolon * Blood transfusion * Transplant o Solid organ o Musculoskeletal allograft tissue Tapeworms (Cestodes) * Adult worms inhabit GI tract of definitive vertebrate host * Larvae inhabit tissues of intermediate host * Humans o Definitive for T. saginata o Intermediate for Echinococcus granulosus (hydatid) o Both definitive and intermediate for T. solium * Adult worms shed egg-containing segments in stool ingested by intermediate host larval form in tissues Taenia saginata * Ingestion of raw or poorly cooked beef * Cows infected via the ingestion of human waste containing the eggs of the parasite * Cows contain viable cysticercus larvae in the muscle * Humans act as the host only to the adult tapeworms * Up to 25 meters in the lumen of intestine * Found all over the world, including the U.S. Beef Tapeworm Treatment * Praziquantel * Albendazole * Niclosamide Cystercercosis * Human infected with the larval stage of Taenia solium * Humans can serve as definitive or intermediate host * Eggs are ingested, or possibly get to stomach by reverse peristalsis * Probably much more common than is reported, since most infections are asymptomatic Cystercercosis * Symptoms depend on location of cysts, but frequently include motor spasms, seizures, confusion, irritability, and personality change * In the eye, often subretinal or in vitreous. Movement may be seen by the patient. Pain, amaurosis, and loss of vision may occur. * Clinical manifestations Cysticercosis * Diagnosis o CT and MRI preferred studies + Discrete cysts that may enhance + Usually multiple lesions # Single lesions especially common in cases from India + Older lesions may calcify o CSF + Lymphs or eos, low glucose, elevated protein o Serology + Especially in cases with multiple cysts Cysticercosis * Treatment o Complex and controversial o Praziquantel and albendazole may kill cysts, but death of larvae can increase inflammation, edema and exacerbate sxs o When possible, surgical resection of symptomatic cyst is preferred o Corticosteroids vs. edema and inflammation; antiseizure meds Babesiosis * Babesiosis caused by hemoprotozoan parasites of the genus Babesia * >100 species reported
* Few actually cause human infection
* Babesia microti
* Life cycle involves two hosts:
o Deer tick, Ixodes dammini, (definitive host) introduces sporozoites into white-footed mouse
* Once ingested by an appropriate tick gametes unite and undergo a sporogonic cycle resulting in sporozoites
* Humans enter cycle when bitten by infected ticks
Deer are the hosts upon which the adult ticks feed and are indirectly part of the Babesia cycle as they influence the tick population
* Clindamycin* plus quinine
* Atovaquone* plus azithromycin*
* Exchange transfusion in severely ill patients with high parasitemia

Classification of Parasitic Diseases
* Protozoa: amoeba; flagellates; ciliates; apicomplexa; microspors (primitive intracellular parasites)
* Metazoa (two phyla)
o Helminths (worms)
+ Nematodes
# Intestinal
# Extra-intestinal
+ Flatworms (platyhelminths)
# Cestodes (tapeworms)
# Trematodes (flukes)
o Arthopods (ectoparasites): scabies, lice, fly larvae

General rules of treatment
* Protozoa: require species-specific treatment
* Metozoa: species-specific

General rules of treatment of metazoa
Nematodes
Intestinal
Mebendazole or Albendazole
Tissue
Albendazole
Filiariae
Ivermectin, doxycycline
Cestodes
Praziquantel, Albendazole, Niclosamide
Trematode
Praziquantel
Ectoparasites
Permethrin, Ivermectin
This is just the beginning of a great adventure in infectious diseases
Sine qua non:history and physical examination

Emerging Infections and Medical Procedures.ppt

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