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Terminology
Host
Infection/colonization
Commensalism
Mutualism
Parasite
Pathogen
Pathogenicity
Saprophytes
Opportunistic
Antigen
Definition
Organism capable of supporting the physical, growth, and nutritional requirements of another organism
Multiplying of the organism on the host
Both organism and infection live together without hurting each other
Both organism and host benefit
The parasite benefits at the expense of the host
An agent that can cause disease
The ability of an organism to cause disease
Organisms that thrive on dead or decaying matter (ex. maggot)
Organism that only produces disease when the host immune system is compromised
Anything capable of provoking an immune response
Classifications of Infectious Disease
Epidemiology
Incidence/prevalence
Endemic
Epidemic
Pandemic
how many new cases over a period of time/number of people who have the disease at a particular time
Incidence and prevalence are stable
Increased incidence
Spread of disease beyond continental boundaries
Portal of Entry into the Body
Penetration
Direct contact
Ingestion
Inhalation
crosses the boundaries of mucus membranes or skin
physical touch of infectious material
eat the bacteria
breathing in droplets of organisms
Source
Endogenous
Exogenous
In the body; Patients own microbial flora
1. Feces, blood, body fluids, respiratory secretions and urine
2. Zoonoses: from animal to human
3. Nosocomial: health care facility
4. Community Acquired
5. Inanimate objects: fomites
Symptoms
Clinical presentation
Specific or nonspecific symptoms
Some require lab testing (WBC, hepatitis)
Disease
Incubation Period
Prodromal Stage
Acute Stage
Convalescent Stage
Resolution Stage
Toxins
Adhesion Factors
Evasive Factors
Invasive Factors
Culture
Serology
Direct Antigen
Detection
DNA and RNA
Antimicrobials
pathogen begins active replication without producing recognizable symptoms in the host
initial appearance of symptoms in the host (non-specific)
rapid proliferation and dissemination of the pathogen (specific symptoms)
containment of infection and progressive elimination of the pathogen
complete elimination of the organism
Virulence Factors (ability to cause disease)
alters and destroys the normal functions of the cells
the ability to attach to tissue for infection
factors that are produced by organism so the host cannot eliminate it (slime layer, capsule)
the organism produces these inside to damage the host
Diagnosis
sputum, wound; looking for bacteria
look for antibodies against antigen (IgG, IgM)
purified antibodies from animals used to detect antigens of infectious agents in specimens obtained from the
host
identification
Treatment
1. Antibacterials
2. Antivirals
3. Antifungals
4. Antiparasitic agents
Immunotherapy
Surgical
Increase host immune response
Removal of infected tissue
Infectious Disease Agents
Prions
Viruses
Protein particles that lack DNA/RNA
Known as spongiform encephalopathies because of appearance of post-mortem brain w/large vacuoles in the cortex and
cerebellum
Include: Creutzfeldt-Jakob disease (brain shrinkage); All produce neurodegenerative disease (ataxia, syncope, dementia, death)
o Can’t replicate outside cell
o Can insert genome into host cell chromosome
o Protein coat surrounding DNA/RNA
o Virus infection and replication
o Some are shed in envelopes of cell membrane
o Smallest obligate intracellular parasite
o Use biosynthetic machinery of cell to
operate
Capsule
Endotoxins
Exotoxins
Invasive/Adhesion
factors
Bacteria
Characteristics of Bacteria: Contain DNA and RNA
gelatin layer polysaccharide covering the entire bacterium
Lipopolysaccharide (activate host complement pathway)
proteins released from bacterial cell during growth
Enzymes that the cell produces
Type of Bacteria
Gram positive cocci
Purple Sphere
Gram positive rods
Purple Rod
Gram negative rods
Red Rod
Gram negative Cocci
Red Sphere
Streptococcus
Staphylococcus
Clostridia (tenaus, botulism, gas gangrene)
Lesteria monocytogenes
Most enteric bacteria
1. E. coli
2. Campylocbacter
3. Pseudomonas
4. Salmonella
5. Shigella
6. H. flu
1. Neisseria gonorrhoeae
2. Neisseria meningitides
3. M. Cat
Produce a Rigid Peptidoglycan Cell Wall
Rickettsiae
Chlamydia
Ehrlichiae
Rocky mountain spotted fever
Go into cell and replicate. Includes STDs, ocular infections, pneumonia of newborns, some upper respiratory
infections
Obligate intracellular organisms, tick vector
Fungi
Two groups
Produces
Yeast
Mold
Cell wall unlike the petidoglycan of bacteria
Parasites
Benefits from biological relationship with another organism
Protozoa
Helminthes
Ectoparasites
Unicellular animals with nucleus and organelles
Includes: malaria, amebic dysentery, giardiasis
Nematodes or roundworms, tapeworms, flukes
Ingestion of fertilized eggs or penetration of larva through the skin
affect outside
tick, scabies, lice
cause localized inflammation of body
Bioterorism
1. B. anthracis (Anthrax)
2. Yersinia pestis (Plague)
3. Smallpox
4. Hemorrhagic Fever (Ebola)
5. Clostridium botulinum toxin
Global Infectios Disease
West Nile Virus
Severe Acute Respiratory Syndrome
Flavirus
China
Highly transmissible
Lyme’s Disease
Borelia burgdorferi (spirochete)
Caused by:
Ixodidae scapularis (deer tick)
Transmitted primarily by:
2 years
Life span:
Once
Through each developmental stage feeds:
Most cases are transmited through this stage:
Nymph stage (very small size less than 2mm)
White-footed mice, white-tailed deer, humans
Spirochete’s reservoir and tick hosts include:
Person
Nymphs are most likely to feed on:
Mid-gut of unfed ticks
Spirochetes reside in:
First 24hours of feeding to tic’s salivary glands
Spirochetes travel during:
3-32 days
Incubation period is:
Pathophysiology of the disease occurs through combination of: Organism-induced local inflammation, cytokine release, autoimmune
Stage 1
Erythema migrans
Large, red, painless, expanding, annular, well-demarcated
maculopapular target-shaped “bulls-eye” lesion:
Eryhthema migrans occurs in areas such as:
Untreated rash lasts:
Rash is due to:
Thigh, axilla, groin
2-3 weeks
Immune systems reaction to spirochetes
Stage 2
The involvement of:
One or more organ systems (occurs days to weeks after bite; intermittent
and fluctuating w/eventual disappearance)
o H/A
o Neck stiffness
o Myalgias
o Arthralgias
o Fatigue
o Malaise
o LAD
o Chills
o Low grade fever
**Neurological and Cardiac
o Bell’s palsy
o Pericarditis, carditis
o Peripheral neuropathies
o AV block, encephalitis
o Arthritis, orchitis, hepatitis
o Aceptic meningitis
Iritis, keratitis, optic neuritis, uveitis
Psychosis, memory loss, dementia, depression, sleep disorders
Constitutional flu-like symptoms
The most common disease are:
Clinical manifestations:
Opthalmic manifestations:
Neuropsychiatric symptoms:
Stage 3
Acrodermatitis chronic atrophicans
Reddish purple plaques and nodules evolving to atrophic
lesions located on the extensor surfaces of the legs:
Clinical manifestations:
Initial test is:
If positive, Elisa is followed by a:
Culture of CSF when neurological findings are present shows:
Other diagnostic tests:
1. Arthritis (untreated patients)
2. Chronic neurological syndromes
Elisa for IgM and IgG B Burgdorferi antibodies
Western blot test (peak 3-6 weeks after onset of symptoms)
Mild pleocytosis, increase protein, decrease glucose
EKG ST elevation (Pericarditis) and AV Block
Elevated ESR, AST
CBC- Leukocytosis
Treatment
Stage 1:
Doxycycline or Tetracycline PO x 14-21 days CI in children <12 or preg.
Amoxicillin, Cefuroxime (Ceftin) or Erythromycin PO x 14-21days
Doxycycline, Amoxicillin PO x 28 days
IV ceftriaxone (Rocephin) or penicillin G x 3-4 weeks
Daily steroids and aspirin
NSAIDS
Stage 1 Alternative:
Stage 2 & 3- Normal CSF:
Stage 2 & 3- Meningitis:
For refractory conduction abnormalities:
For arthritis:
Progressive, rapid ascending flaccid paralysis:
Caused by:
Secreted by:
The median days on the host is:
Begins in the:
Ascends to the:
Neurotoxin interferes with:
Most common in:
Two species that most commonly cause tick paralysis is:
Treatment:
Tick-bite paralysis
Neurotoxin
Tick that has fed for several days on the host
6
Feet and legs
Face, tongue and pharynx (sometimes ending w/resp failure and death)
Motor nerve conduction
Children <7
Wood tick and American dog tic (infx site is usually the scalp)
Pt recovers completely in hours to days after tic is removed
Rocky mountain Spotted Fever
Most common fatal Tick born disease in the US; Acute, potentially fatal infection
Caused by:
Transtmitted via
Onset of symptoms is typically:
Pathophysiology- Vasculitis due to:
Damage to vessels results in:
Triad:
Clinical maniefestations
Rash
Pulmonary
Gastrointestinal
Neurological
Diagnosis:
Electrolytes, LFTs, BUN/Cr, glucose shows:
Treatment
In pregnant and allergic patients or those with CNS
manifestations use:
Severe cases complicated by extensive vasculitis,
encephalitis, or cerebral edema use:
Acute infection with:
Transmitted via:
Most the most commonly indicated transmitter is:
Infection results in necrotic areas in the:
Granulomas form which may coalesce to form:
Classical clinical finding:
Clinical Manifestations:
Rickettsia rickettsii (intracellular bacteria)
Dermacentor tick vector (between April and September)
1 week after the tick bite
Direct endothelial cell invasion and bacterial multiplication
Increase vascular permeability
Micro-hemorrhage
Complement activation
Microinfarcts w/secondary thromboses
Tissue necrosis
Fever, rash, headache
Generalized edema
N/V, dehydration
Hempatosplenomegaly
Malaise
Myalgia, arthalgia
Conjunctivitis
photophobia
Erythematous maculopapular rash blanches under pressure
Begins peripherally and spreads centrally
Non-productive cough, chest pain, dyspnea, and rales
N/V, abdominal pain, distension,a nd illeus
Focal or generalized neuro symptoms, meningismus, H/A, encephalitis, delirium
Acute and convalescent serology, immunofluorescent staining of skin biopsy
CBC: normal WBC count, anemia
Hyponatremia, increase AST &LDH, hyperbilrubinemia
o Fix fluid/electrolyte deficits
o Tylenol for fever
o Oxygen therapy
o Doxcycline/Tetracycline x 7days
Chloramphenicol
High dose steroids
Tularemia
Francisella Tularensis (gram-negative pleomorphic coccobacilli)
Tick, fly, mosquito, and cat bites
Cutaneous inoculation through skin lesions, aerosol inhalation or ingestion
Rabbits and ticks
Liver, spleen and other organs (surrounded by PMNs)
abscesses
Ulcer at the site of inoculation/painful regional LAD
o Abrupt onset of fever
o N/V/D
o Headache
o Anorexia
o Chills
o Abdominal pain
Six forms of Tularemia (Each form represents mode of Transmission)
Large tender regional LAD w/red painful papule, reactive nonhealing ulcer (transmitted via tick bites or animal contact):
Tender regional LAD w/no local lesions or ulcers (entry through
Ulceroglandular
Glandular
conjunctiva causing a unilateral conjunctivitis):
Unilateral purulent conjunctivitis, preauricular or cervical LAD
Exudative pharyngitis w/ulceration and regional LAD
Ocular glandular
Oropharyngeal
(contaminated food and water; contact with GI tract):
Fever, sepsis, pulmonary disease, diarrhea, bowel necrosis, no
ulcer (systemic febrile illness, fulminating sepsis,
Typhoidal
pleuropulmonary disease):
Fever, dry cough, pleuritis (sheep shearers, farmers, lab workers):
Chest x-ray of the pulmonic form shows:
Diagnosis is based on:
Gram-stain and culture from wound or blood shows:
Elevated antibody titer with skin ulcer for 2 weeks:
Not positive until the second week of illness:
Rapid diagnosis:
Treatment- first line agent:
For tularemic meningitis:
Chronic painful regional LAD persisting for several weeks or
months after a scratch or bite from a flea-infested cat:
Caused by:
Infection may disseminate and produce more:
Clinical manifestations:
Pathology:
Pathologic examination of the involved nodes shows:
Serologic tests in patients with intact immunity are:
The highest diagnostic sensitivity is:
Treatment for cases of typical CSD:
Treatment for encephalitis is:
Pulmonic
Lobar infiltrate, hilar adenopathy, pleural effusion, military
pattern
Clinical manifestations/serologic studies
Gram negative coccobacilli
Agglutinin Titers (four-fold rise in second titer obtained 2 weeks later
confirms diagnosis)
ELISA
Polymerase chain reaction of purulent specimens
IM streptomycin or gentamicin
Add chloramphenicol or ceftriaxone
Cat scratch disease
Bartonella Henselase (gram negative bacillus)
Generalized LAD and systemic manifestations
Localized papule progressing to pustule (crusts 3-5 days after cat scratch
with tender regional LAD w/in 1-2 weeks after inoculation)
granulomatous inflammation with necrosis, microabscesses, no
evidence of angiogenesis (tumor)
small pleomorphic gram negative bacilli
Positive
**PSR assay on lymph node biopsy
Doxycycline, ciprofloxacin, zithromax PO
IV gentamicin
Malaria
(Most deadly vector born disease in the World)
Acute and chronic protozoan infection transmitted by:
Accounts for 95% of malarial infections worldwide:
Transmitted via:
Parasites derive their energy solely from glucose causing:
Travels in bloodstream to:
Replicate inside cell causing:
They suppress:
Clinical manifestations:
**Classic signs:
Bite of female Anopheles mosquito
Plasmodium falciparum and vivax
Mosquito saliva during feeding
Hypoglycemia and lactic acidosis
Liver (remain dormant)
Lysis and release of pro-inflammatory cytokines (*cyclical patter) causing
sludging of blood and localized necrosis
Hematopoiesis and increased clearance of RBCs by spleen
o Fever, chills
o Diaphoresis
o N/V/D, cough
o Hepatosplenomegaly
o Abd. pain
o Malaise, H/A
o Anemia
o Myalgias
o Tachycardia
o jaundice
o fatigue
o hypotension
Shivering chills for 1-2hrs followed by high fever, then excessive
diaphoresis and return to normal body temp more than once a day
P.vivax and P. ovale
Incubation period up to:
12 months (high fever every 48hrs)
2-3months
Liver
Infestations may resolve without treatment after:
Relapse comes from the:
P. malariae
Incubation period is approximately:
Dormant parasites in RBC causes reinfection:
May become chronic and cause:
35days (fever every 72 hours)
Recrudescence
Nephrotic syndrome
P. falciparum
Incubation period is usually:
Highest occurrence in:
**Death from malaria usually limited to:
Gold standard diagnosis:
Microscopy to evaluate for intracellular parasite forms:
Species:
Admission guidelines:
Patients treated on outpatient basis with adequate follow up
care are:
The drug of choice for non-resistant strains of Plasmodium
species is:
Used to prevent relapse from liver:
Used in chloroquine resistant infections:
Indicated for severe or complicated malaria
12-24 days (high fever every 48hrs w/in 2 months of infx)
Sub-Saharan Africa
P. falciparum infx (has ability to cytoadhere to RBC tendthelium causing
clumping and vaso-obstruction)
*Giemsa-stained thick/thin smear prep every 6-12hrs x 3hrs
It’s best to obtain blood during or right after fever spike
Specific PCR and indirect fluorescent antibody (practical for clinical lab)
P. falciparum, children, pregnant women, immune-compromised
P. vivax, ovale and malariae
Chloroquine PO (inhibits parasite growth by increasing internal pH of
parasite, inhibiting Hgb utilization and metabolism)
Primaquine PO
Quinine sulfate + doxycycline/tetracycline or clindamycin
IV quinidine gluconate + doxycycline or clindamycin
Parasitic Infections
Protozoa and Helminths
The class of parasitic infectious agents is divided into two parts:
Single celled animal that characteristically divides and
Protozoa
multiplies as a host:
Protozoa is transmitted through:
Direct fecal/oral route (don’t cause eosinophilia)
Entamoeba Histolytica, Naegleria, Acanthamoeba
Amoeba:
o Giardia lamblia
o Balantidium coli
Protozoa:
o Cryptosporidium
o Trichomonas vaginalis
Infection with the intestinal protozoan:
Pseudopod forming, non-flagellated protozoan parasite that
exerts:
Acquired by:
Released from cysts in the small intestine and, in most pts,
remain as harmless inhabitants of the large bowel:
in others the trophozoites invade the bowel mucosa causing:
Abdominal pain x several weeks, bloody diarrhea, weight loss
and fever
Signs of liver abscess:
Infectious cysts are shed in the:
Diagnosis- on stool examination:
Other tests:
Treat asymptomatic colonization with:
For liver abscess:
For invasive disease treatment:
Amebiasis
Entamoeba histolytica
A lytic effect on tissue
Ingestion of viable cysts from focally contaminated water, or
hands, and food
Motile trophozoites (after 12months)
symptomatic colitis, bloodstream (causing distant abscesses of the
liver (MC), lungs, or brain)
Amebic colitis
Jaundice, hepatomegaly, RUQ pain, 1-2wk hx of fever
Stool
Trophozoites or cysts
ELISA, RUQ US or CT for liver abcess, Colonoscopy w/biopsy
Luminal agent (Iodoquinol, paromycin) (ris factor for development of
invasive disease)
Surgery- drain abscess
Metronidazole + iodoquinol
Free-Living Amoeba
(found in wide variety of fresh and brackish water incl. lakes, taps, hot springs, pools, heating and air condition units)
Naegleria fowleri
trophozoites or cysts
olfactory neuroepithelium and subarachnoid space
rhinorrhea of smell, frontal headache, regular signs of meningitis
Severe hemorrhagic necrosis of brain with purulent meningitis
Elevated opening pressure
**Motile trophozoites
Amphotericin B and Rifampin
Primary amebic meningoencephalitis:
follows the aspiration of water contaminated with:
Leads to invasion of:
Causes:
Highly phagocytic, ingests RBCs and brain tissue resulting in:
Lumbar puncture shows:
Wet mount of CSF fluid shows:
Treatment:
Acanthamoeba found in swimming pool water (three syndromes)
Occurs after hematogenous spread of the amoebae from
pulmonary or skin lesions to the CNS or may enter directly via
olfactory epithelium:
Signs and symptoms of G.A.E.:
Insidious onset w/incubation period of:
Diagnosis- LP with CSF analysis shows:
Involves skin, sinus, and pulmonary infections:
Signs and symptoms:
Diagnosis of DGA:
Minor corneal trauma and contact lenses:
Signs and symptoms of AK:
Diagnosis:
If corneal specimens are unremarkable:
Treatment- keratitis:
Treatment- Meningoencephalitis
Granulmatous Amebic Encephalitis
o Mental changes
o Seizures, N/V
o Hemiparesis
o visual changes
o Fever, H/A
o Meningitis, ataxia
Weeks to month
Lymphocytic pleocytosis, increase protein, decrease glucose
Disseminated Granulomatous Amebic Disease
o Ulcer
o Nodules
o Subcu. Abscess
o Sinusitis
o Pneumonitis
Biopsy and culture areas of involvement
Amebic keratitis
o Red eye
o Tearing
o Intense pain
o Foreign body sens.
o Photophobia
o Blurred vision
Wet mount of corneal scrapings or biopsy (demonstrate motile
trophozoites)
Culture contact lenses and solution
Topical miconazole with neomycin, opthamologist
o Sulfadiazone
o Rifampin
o Ketoconazole
o Bactrim
Giardiasis
Major diarrheal disease found throughout the world; MC identified intestinal Parasite in US
Caused by:
Damage to:
Alteration of:
Inhibition of:
This disease does not spread:
Reservoirs:
Signs and symptoms:
Stool examination shows detection of:
Treatment:
ingestion of cysts that release organisms into the small bowel,
colonization of small bowel
Pathophysiology
Endothelium, enterotoxins, immunologic reaction
Gut motility and fluid hypersecretion
Disaccharidase activities
Hematogenously
Beavers, dogs, cats
*Explosive, malodorous, greasy-watery diarrhea
o foul flatus
o abd. Cramps
o sig. malabsorption
o N/V, fever
o weight loss
o lactose intolerance
Parasite or cysts in feces (negative fecal WBCs)
Flagyl or Metronidazole
Cryptosporidiosis (Parasitic disease)
Consumption of cysts
Acquired through:
Self-limited diarrhea
Liberate and infect intestinal epithelial cells causing:
Children <5years
Peak incidence is in:
AIDS or other immunodeficiency
Can be severe in persons with:
o Watery diarrhea o Abd. Cramps
Signs and symptoms
o
Anorexia, fever
Stool examination for:
Treatment:
Infection with:
Caused by:
Reservoirs:
Signs and symptoms:
Stool examination, wet smear shows detection of:
Treatment:
Caused by:
Signs and symptoms:
Wet mount of genital secretions to detect:
Treatment:
Cysts (antigen detection assays)
Nitazoxanide (Alina) or paromomycin (Humatin) + azithromycin
for HIV patients
Blantidiasis
Balantidium coli (ciliated parasite)
Ingested cysts
Pig
*Watery, bloody, mucoid diarrhea
o N/V, dehydration o Abdominal Pain
Cyst or organism in stool
Tetracycline 1st line, metronidazole 2nd line
o Anorexia, wt. loss
Trichomoniasis
Trichomonas vaginalis
*Thin frothy yellow malodorous discharge strawberry cervix
o Itching
o Dysuria
o dyspareunia
Motile organisms (urine antibody tests)
Metronidazote
Helminths (worms)
Multi-cellular animals that usually do not multiply within host, associated with eosinophilia
Elongated, symmetric roundworms that predominantly
Nematodes
infect either intestines or tissues:
o Ascaris lumbricoides
o Strongyloides stercoralis
Organisms:
o Necator americanus
o Trichinella spiralis
o Ancylostoma duodenale
o Enterobius vedrmicularis
o Brazillense
o Trichuris trichiura
o Toxocara canis/cati
Most common intestinal and largest intestinal nematode:
Ascariasis- Ascaris lumbricoides
1. ingestion of cyst in feces-contaminated soil
Pathology:
2. larvae released in intestine and invade mucosa
3. migrate to pulmonary bed via portal veins
4. migrates up bronchi, cough up, swallowed
5. mature and lay eggs in intestines
6-24 months
Adult worms live in the gut for:
o Pancreatitis/appendicitis o Cholangitis
o Bowel obstruct.
Adult worms may cause:
Not self infectious
Eggs passed in the feces and embryonate in the soil is:
They secrete a tripsen factor in the intestine which prevents: Digesting proteins which they eat
o Non-productive cough
o Fever
o Hempoptysis
Signs/Symptoms- early:
o Substernal chest pain
o wheezing
o Dyspnea
Eosinophilia, pneumonitis w/transient CXR changes
Diagnosis- early infx:
Detection of eggs or worm in feces, abd x-ray or CT w/contrast
Diagnosis- Late infx:
Albendazole, mebendazole, ivermectin
Treatment that Kills worm:
Piperazine, pyrantel
Treatment that Causes spastic paralysis:
Two species:
Most common cause of exposure:
Worms use teeth or cutting plates to attach to the:
Ancylostoma lives:
Necator lives:
Disease develops due to:
Hookworms
Necator americanus and Ancylostoma duadenale
Walking bare foot in contaminated soil
Small bowel mucosa (and suck blood)
1 year
5 years
1. heavy warm burden
2. prolong duration of infx
Signs/Symptoms:
Diagnosis:
Treatment:
Skin eruption caused by:
Infection occurs after skin contact with:
Larvae penetrate skin causing:
Diagnosis:
Treatment:
3. inadequate iron intake
Rash at entry
Fever, cough
Transient
Inflam. diarrhea
Epigastric pain
pneumonitis
Eosinophilia, inron deficiency anemia, eggs and worms in feces
Albendazole, mebendazole and iron replacement
Cutaneous Larva Migrans
Burrowing larvae of hookworms, Ancylostoma brazillense
Soil contaminated with cat and dog feces
Intensely pruritic erythematous lesions (then linear or tortuous tracts as
they migrate advancing several cm/day)
Clinically established, in biopsy/presentation
Thiabendazole, albendazole, mebendazole, ivermectin
Visceral Larva Migrans
Caused by:
Nematodes (normally parasitic for domestic animal hosts)
Host tissues
In humans the larvae migrate through:
Preschoolers who eat dirt
Classically occurs in:
Toxocara canis and cati
Due to egg or larva ingestion contaminated w/cat or dog
feces:
Larvae invade intestinal mucosa and spread to:
Liver, lungs, CNS and other sites (provoking inflammation)
o Fever, Cough
o Anorexia
o Weight loss
Signs/Symptoms:
o urticaria
o Wheezing
o hepatosplenomegaly
Eosinophilia, leukocytosis, ELISA, transient pulmonary infiltrates on
Diagnosis:
CXR
self-limited, steroids for severe inflam., mebendazole, albendazole
Treatment:
Strongyloidiasis
Distinguished by it’s ability to:
Replicate in human host (permitting ongoing autoinfection)
Strongyloides
Only helminth to secrete larvae in feces:
Soil
Can undergo a free-living cycle of development in the:
Larvae may penetrate bowel wall and travel throughout body CNS, liver, and lung disease
causing:
o Ground itch
o Larva currens
o Wheezing
Signs/Symptoms:
o Anorexia, weight loss o Wheezing, cough
o Abd. pain, N/V/D
Demonstration of larvae in feces, eosinophilia
Diagnosis:
Ivermectin, thiabendazole
Treatment:
Caused by:
Occurs after ingestion of:
Parasite is liberated in:
Travels via:
Causes
Reservoir:
Signs/Symptoms:
Diagnosis:
Treatment:
Treatment for severe myositis:
Trichinosis
Trichinella Spiralis
Meat containing cysts
Small intestine (invades mucos)
Bloodstream to tissues (affinity for striated muscle fibers cause developmental
arrest)
Myositis and myocarditis
Domestic pigs
o Severe enteritis o Periorbital edema
o Myositis, urticaria
o Fever, rash
o Hypersens. Rxn
o Myocarditis w/
o Pneumonitis
o encephalitis
dysrhythmias
o Eosinophilia
o Myglobinuria
o Larvae on muscle
o Elev. AB titer
o CK elevated
biopsy
Mebendazole, albendasole
steroids
Enterobiasis (Pinworm infection)
Lives in:
Small intestines (primarily ileocecal region)
Gravid female migrates to anus and deposits eggs in:
Perianal skin folds (usually at nighttime)
3 weeks without hatching
Ova may survive for up to:
Air, fomites, mouth, anus
Eggs can be released in
o Asymptomatic
o Perianal pruritus
o Perianal
Signs/symptoms:
o Weight loss
o Abd. Pain
excoriations
o vulvovaginitis
o Pelvic pain
Scotch tape to perianal region in morning shows eggs
Diagnosis:
Albendazole, mebendazole
Treatment:
Infection with:
Feeds on:
Hatch in:
Reside in:
Transmitted via:
Signs/symptoms:
Diagnosis:
The drug of choice is:
Trichuriasis
Whipworm
Tissue secretion (not blood)
Small intestine
Large intestine (no pulmonary migration or symptoms)
Fecal-oral route, contaminated soil (adults lay eggs from up to 5yrs)
o Abd. Pain
o Anorexia
o Diarrhea
o anemia
o malnourishment
o Rectal prolapsed
Demonstration of whipworm eggs in stool
mebendazole
Trematodes
Flatworms, “flukes”
Human infection is initiated either through:
Life cycle in two hosts:
Organisms:
Unlike other trematodes, schistosomes have:
Humans infected while:
Transforms in human host to travel through:
Becomes adults in:
Live together and lay eggs in:
Penetrate vascular endothelium and enter the:
Signs and symptoms:
Intestinal species:
Vesicular (causes bladder cancer):
Diagnosis/labs:
Drug of choice is:
Direct penetration of intact skin or ingestion
1. Definitive (humans, domestic and wild animals)
2. Intermediate (freshwater snail)
o Schistosoma sp. (blood)
o Clonorchis & Fasciola sp (liver)
o Paragonimus (lung)
o Fasciolopsis buski (intestine)
Schistosomiasis
Separate sexes
Swimming
Venous circulation to heart, lungs and portal circulation
3 weeks
Genitourinary or gastrointestinal veins
Bladder or bowel
o Katayma fever- serum sickness
o Fever, LAD
o Dermatitis at entry
o Hepatosplenomegaly
o GI and hepatosplenic disease
o Portal HTN
o Bloody diarrhea
o Abdominal pain
GU disease, dysuria, frequency, hematuria
o Eosinophilia
o UA
o Stool
o antiodies
o FAST-ELISA
examination
praziquantel
Clonorchiasis:
“Chinese liver fluke”
Larva released into:
Transmitted by:
Feeds on:
Treatment:
Duodenum (enters biliary duct and matures)
Fresh water undercooked fish
Mucosal secretions (lays eggs)
Albendazole, praziquantel
Fascioliasis
“Sheep liver fluke”
Aquatic plants
Biliary disease
Duodenum
Intestinal wall, peritoneum, and liver capsule (reaches biliary ducts)
o Fever, RUQ pain
o Hepatomegaly
o Weight loss
o Biliary obstruction
o Ascend. Cholangitis
o Anemia
Eosinophilia, Stool examination, ELISA, increase LFTs
*Bithionol
*Triclabendasole (praziquantel is also used)
Transmitted from:
Causes:
Larva released in:
Penetrates:
signs/symptoms:
Diagnosis
Drug of choice is:
Second line drug of choice is:
Lung fluke (paragonimus)
Westermani
Most common thic, fleshy, reddish-brown, egg0shaped worm
Humans, foxes, wolves, and various feline hosts
Inhabits lung parenchyma of:
Eating undercooked freshwater crab or crayfishcontaing cysts
Acquired by:
Intestinal wall, peritoneum, diaphragm
Migrate through:
Lungs
Mature in the:
Sputum and feces
Eggs passed in:
Acute phase of infection
Death may occur during:
1-2months
Spontaneous recovery in:
o Abd. Pain
o Diarrhea, fever
o SOB, CP
Signs/symptoms:
o pneumonia
o Bronchitis, hemoptysis
o Lung abscess
Extrapulmonary:
From migration to various organs (liver, spleen, CNS, intestine)
Eosinophilia, eggs in sputum or stool, ELISA
Diagnosis:
praziquantel
Drug of choice is:
Intestinal fluke
Fasciolopsis buski
Ingestion of fresh water aquatic plants
Duodenum and jejunum of pigs and humans
Inflammation, ulceration, and mucous secretion
o Asymptomatic
o Diarrhea
o Weight loss
o malaise
o Abd. Pain, N/V/D o Hunger pains
Stool examination shows ova and worms, eosinophilia
praziquantel
Most common intestinal nematode:
Acquired during:
Giant fluke found in:
Causes:
Signs/symptoms:
Diagnosis
Drug of choice is:
Cestodes
(long segmented tapeworms)
Attaches to intestinal mucosa via:
Adults reside in:
Larva can be found in:
As it matures each segment is:
Eggs ingested via contaminated soil by:
Primary host ingests:
1. Beef tape worm (common among cattle and humans):
2. Treatment:
1. Pork tape worm (common in pigs, humans, dogs, cats, sheep):
2. Treatment:
T. solium, larvae migrate and infect CNS, skeletal muscle,
subcutaneous tissue or eye:
Diagnosis:
Sucking cups on scolex
GI tract
Any organ
Displaced further back
Intermediate host
Intermediate flesh (intestinal tract)
1. Taenia saginata
2. Niclosamide, Praziquantel
1. Taenia solium
2. Praziquantel, steroid, surgery
Cysticercosis
Eosinophilia, stool examination for demonstration of eggs or
segments in feces, serology
Hemoflagellates
Flagellated protozoa that are parasitic in blood and tissues
Leishmania
Transmitted by:
Causes:
Injected into skin of host, pass into the:
Location of lesions determined by:
Visceral disease:
Mucocutaneous disease:
Diagnosis:
Drug of choice is:
Second line drug of choice is:
“American trypanosome”
Trypanosoma cruzi transmitted by:
Clinical manifestations:
Mortality due to:
Diagnosis:
Treatment:
Bite of female sandfly
Visceral and mucocutaneous disease
Blood and tissues
Temperature
*Kala-azar= black fever skin turns gray, cachectic, fever
Hepatosplenomegaly
Fever, cachectic
Pancytopenia
Papule at bite site, regional LAD, ulcerative lesions
Shows pathogen w/biopsy + Gemsa stein
Antimony
Amphotericin B (can also use pentamidine)
Trypanosoma
Chagas disease
Reduvid bugs feces expelled when feeding via breaks in the skin,
mucus membranes, or conjunctiva
o Lesion at site of
o Acute fever
o Malaise, edema
entry
o Anorexia, LAD
o Myalgia, GI dis.
o hepatosplenomegaly o encephalitis
o Muscu. invasion
Chronic cardiomyopathy
Demonstration of parasite on blood smear, EKG
Benznidazole
African Sleeping Sickness
Transmitted by:
Tsetse fly bite trypanosma bruceri rhodesiense and gambiense
Blood and lymphatic system
Painless skin chancre at bite followed by dissemination via:
Systemic febrile illness and then to CNS, widespread LAD and
Causes:
splenomegaly
o Anemia, thrombocytopenia
o lymph nodes
Diagnosis:
o Detect parasite in blood
o sinwith Giemsa-stained smear
Suramin
Treatment- early (skin):
Organic arsenicals
Treatment – late (CNS):
HIV and AIDs
The US in the summer of 1981
HIV (family of human retroviruses)
1. Human T lymphotropic viruses HTLV-I and HTLV-II
 (transforming retroviruses; oncogencic assc. w/t-cell lymphoma)
2. Human immunodeficiency viruses, HIV-1 and HIV-2
 (cytopathic viruses- not directly oncogenic)
HIV-1
In the US the most common is:
HIV-2
Immune deficiency develops more slowly and is milder and
patients are less infectious early in the course in:
Lentivirus
HIV is a:
The reverse transcription of its genomic RNA to DNA by reverse
Lentivirus is a subgroup of RNA retroviruses whose
transcriptase
hallmark is:
CD4 T-cell lymphocytes
HIV has a high affinity for:
HIV enters the body mainly through:
The mucosal and langerhans cells (trap the antigens)
Chronic and persistent infection
The dissemination of virus to lymphoid organs is a major
factor in the establishment of a:
Lymphoid tissues
The major anatomic sites for the establishment and
propagation of HIV infection is:
The replication cycle begins with the:
Binding of HIV gp120 to the CD4 molecule (receptor on host cell surface)
AIDS was first recognized in:
The etiologic agent of AIDS is:
The 4 recognized human retroviruses belong to 2 distinct
groups:
The gp 120 undergoes a conformational change that
facilitates binding to:
The two major receptors for HIV-1 are
The HIV envelope protein binds to:
HIV RNA is uncoated and internalized into the:
Contained in the infecting virion, catalyzes RNA into
double-strand DNA:
DNA is integrated into the host cell chromosomes through:
What follows this integration is the:
RNA is translated into proteins that undergo:
The viral particle is formed by the:
Catalyzes the cleavage of precursor to yield the mature
virion:
At each point in replication cycle there’s a potential for:
As the immune system response to the initial infection, viral
titers:
Stops fusion through cell:
Directly stops reverse transcriptase:
incorporate into DNAase blank genes, so transcription can’t
go further:
No cleavage in assembly of mature virant:
The hallmark of HIV is the:
The amount of CD4+ cells lost yearly initially is:
Massive HIV production is linked with destruction of:
Transmission:
HIV is transmitted primarily through:
HIV concentrates in seminal and vaginal fluid, particularly
in situations where there’s:
Chief predictor of heterosexual transmission of HIV was the
level of:
HIV is isolated in low titers from:
Use of antiretroviral drugs as post-exposure prophylaxis:
During pregnancy HIV can be transmitted during:
Treatment of HIV-infected pregnant woman from 2nd
trimester  delivery and of infant for 6 weeks after birth:
The hallmark of HIV disease is the immunodeficiency from
a progressive deficiency of:
Direct infection and destruction of CD4+ T cells are by:
When number of CD4+Tcells declines below a certain level,
patient is high risk of developing:
HIV patients are categorized on the basis of clinical
conditions associated with:
AIDS-Defining Diseases:
Mononucleiosis-like symptoms appear 2-4 wees after
exposure to HIV:
One of a group of co-receptors
CCR5 and CXCR4
CD2 molecule (shape changes, then fuses w/the host cell and penetrates the
membrane of target cells)
Target cell
Reverse transcriptase enzyme
Integrase (virally encoded enzyme)
Transcription of proviral DNA to genomic RNA
Modification and cleavage
Assembly of HIV proteins, enzymes, and genomic RNA (at the plasma
membrane of the cells)
Protease (virally encoded)
Therapeutic intervention
Decline
Fusion inhibitors
Non-nuc
Nuc (nucleoside anaolog)
Protease inhibitors
Establishment of a chronic persistent infection
30-60
2 billion CD4 cells daily
Semen, blood, breast milk, vaginal fluids
Sexual contact
Increase number of WBCs (genital inflammatory states, syphilis, herpes)
Plasma viremia
Saliva (no evidence of transmission through saliva)
Decreases risk of infection
1st, 2nd, and 3rd trimester
Zidovudine (decreases transmission)
Helper CD4 T cells
HIV and activation-induced cell death
*AIDS-defining illnesses (opportunistic diseases)
HIV infection and CD4+ T lymphocyte counts
1.
2.
3.
4.
5.
6.
7.
Invasive candidiasis
Cryptococcus/histoplas.
Cryptosporidiosis>1month
HSV>1mnth or visceral HSV
Salmonella bacteremia
Dissem. Or extrapulm. MAC
Pneumocystis carinii
pneumonia
Acute retroviral infection
Asymptomatic infection (most transmission occurs)
During this phase pt. becomes seropositive but no clinical
HIV infection
8.
9.
10.
11.
12.
13.
14.
15.
Invasive cerv. Cancer
Extrapulm. Cocidiomycosis
Cytomegalovirus
HIV encephalopathy
Kaposi’s sarcoma
Certain lymphomas
TB, HIV-wasting syndr.
Cerebral toxoplasmosis
evidence of:
Virus is actively replicating and despite absence of symptoms
individuals are:
The higher the CD4 T cell count, the lower the:
Highly infective
Viral load
Symptomatic infection (Pre-AIDS)
Constitutional symptoms (night sweats, fever, chills, weight loss,
diarrhea, rash, fatigue)
AIDS
The first evidence of immune system dysfunction is:
Marked immune infection leading to disseminated
opportunistic infection:
If CD4 T cell <200 may have:
Opportunistic diseases
Laboratory tests
Screening test for detecting HIV-antibody, 1-3 weeks after
exposure:
Specific confirmatory test for positive result:
Best indicator of the status of the immune system and of
risk for opportunistic infections and disease progression:
Immune system is essentially normal if CD4 + lymphocyte
count is greater than:
Most opportunistic infections occur when the CD4 count is:
Best option if screening tests negative:
HIV infectious should be diagnosed using either:
For establishing the diagnosis of infection in infants born to
HIV-1 infected mothers:
If recent high-risk exposure to HIV is suspected the test that
should be obtained is:
ELISA (reported as reactive or non-reactive, sensitivity 99%)
Western blot
CD4 + lymphocyte count
500
Less than 200
Viral load (PCR HIV RNA)
ELISA or rapid testing
PCR and peripheral blood mononuclear cells for HIV RNA or DNA
Baseline antibody test (if negative, repeat at 1, 3, and 6mths)
Clinical Use and Misuse of Antibiotics
Drug that kills sensitive organism causing the organism level to
Bacteriocidal
fall rapidly after it is exposed to the drug:
Microbial metabolism
Induces lethal changes in:
Viability
Blocks activities essential for:
Resistance
Less likely to cause:
Includes:
Most drugs (beta lactams, quinolones, aminoglycosides, macrolides)
Drug that inhibits growth of bacteria but does not kill it:
Bacteriostatic
Causes the number of organism to:
Remain relatively constant (after drug exposure)
Eliminate organisms
Require immunologic mechanisms to:
Resistance
More likely to cause:
Sulfonamides and tetracyclines
Includes:
Antimicrobial spectrum
Have activity against a single species or a limited group of
pathogens:
Have activity against a wide range of drugs:
First, always choose:
Determines the exact organism responsible for an infection and
the antibiotics that it is sensitive or resistant to:
Result takes:
Organism is classified as having:
Lowest concentration of the drug that inhibits bacterial growth:
Narrow-spectrum drugs (penicillin)
Broad-spectrum drugs (fluoroquinolones)
Narrowst spectrum (less likely to cause superinfection and development
of bacterial resistance)
Culture and sensitivity
72hrs
1. Susceptibility
2. Intermediate sensitivity
3. Resistance
(based on MIC)
MIC
Mechanisms of Microbial Resistance
Inactivation of drug by:
Decreased accumulation of drug by:
Reduced affinity of the target microbe by:
Microbial enzymes (beta lactamase, AMG)
Microbe (quinolones, AMG)
Drug (Beta lactams, quinolones, macrolides, tetracyclines, AMG)
Multiply itself and thrive despite drug (sulfonamides)
Bacterial cell (beta lactams, quinolones, tetracyclines)
Alteration in microbe so it can:
Increased amount of drug pumped out of:
Factors contributing to resistance
Frequent administration of antimicrobials in either:
Inadequate patient education on:
Availability and marketing of:
Widespread use of antimicrobials in:
Administration of antimicrobials as:
Prescribing broad spectrum vs.:
Unfamiliarity with local:
B-lactam resistance to strep pneumonia is due to:
Inappropriate dosing and duration of:
Selection of appropriate antibiotics
Based on:
Antibiotic choice will be based on:
Used initially until lab results are available:
Pregnancy:
Minor self-limiting or viral infections
Proper use of antimicrobials
Broad-spectrum antimicrobials
Farming and maintenance of livestock
Prophylaxis (in low risk infection)
Narrow spectrum antibiotics
Geographical resistance patterns
Penicillin-binding proteins
Antimicrobial therapy
Type of infection, status of patient, drug properties
Lab results or knowledge of most common organisms
empiric therapy (treat minor URI and UTI)
Penacillin, Cephalosporins, Macrolides
(Pregnancy Cures Menses)
Anaphylaxis to PCN
Metabolize and eliminate drug
Broad spectrum ABX w/ anaerobic coverage
Avoid cephalosporin if pt has history of:
Hepatic or renal impairment affects ability to:
Abscesses:
TB
1 line drugs (C) RIPE
Rifampine
Isonaiazid
Pyrazinamide
Ethambutol
st
Treatment of TB: RIPE w/B6
RIPE x 2mo followed by RI x 4mo
Follow CDC guidelines accord. to mortality/morbidity report
Name
MOA
Liver metabolism- acetylation- phase 2
INH- Isoniazid
300mg daily (PO, Acetylators: break dwon drug
Slow: increase risk for toxicity (md. Eastern pts)
IM)
Fast: quick to reach full potential (jap. Pts)
Rifampin (RIF)
Rifadin
Pyrazinamide
(PZA)
Ethambutol
(EMB)
Streptomycin (2nd
line)
Rifabutin
(Mycobutin) (B)
(for MAC infx)
Clofazimine
(lamprene) (C)
2nd line drugs (reserved for resistant organisms) (D)
Streptomycin
Capreomycin (Copstat)- neprotoxic, ototoxic (bacteriastatic)
Ethionamide (Trecator-SC)- hepatic impairment (bacteriastatic)
Cycloserine (Seromycin)- CNS effects- contraindicated in pts w/
seizers (bacteriastatic)
Tetracyclines + flouroquinolones can also be used (bacteriocidal)
Inhibits RNA synth and broad spect abx
Metabolized in liver via cytP450 inducer
Metabolizes prednisone, B-blockers, sulfonamides, oral
contraceptives, caumadin, etc
Lowers pH too low for growth
Not given alone b/c of resistance
15-30mg/kg QS (max-2g) (PO)
Tuberculostatic
15mg/kg QD (max-1600mg) (PO)
Used when tb is not main dx or is life threatening (HIV,
Mening.)
0.5-1g (max-1g) (QD) (IM, IV)
Used in combo w/ 2 pak, clarithromycin or ethambutol
x 16 weeks
Used for prophylaxis against mycobacterium MAC in
HIV. (300mg PO w/ meals)
Clinical efficacy against TB hasn’t been proven. 100mg
ADR
Peripheral neuritis b/c of pyridoxine decrease
*If on INH- pt must be on 50mg Vit B6
Drug induced hep, high risk>50
monitor LFTs to check for liv dz
Red, orange, brown, urine
Used for: TB prophylaxis, meningitis prevention,
leprosy, endocarditis and legionella pneumonia
600mg (PO, IV)
Hyperurecemia- can cause gout
Hepatoxicity
Given 1st 2mo w/ INH and RMP
Dose related to retrobulbar neuritis (loss of central
vision and color discrimination)- reversible
Nephrotoxic, ototoxic- monitor peaks/troughs
Cant be used to treat TB
TB Prophylaxis: based on PPD results, exposure factors and other risk factors
PPD negative with exposure:
For adults, no treatment initially recheck PPD in 3mo
In all neonates and >5yrs w/ exposure: INH w/B6 10mg/kg daily
x 3mo. Repeat PPD
PPD positive- all pts treat w/ INH: Adults: 6mo, >5: 9mo, HIV, IMmunocompromised: 12mo
Multicellular threadlike hyphae; reproduce by spores:
Unicellular pseudohyphae; reproduce by budding:
Can grow as either mold or yeast depending on temp:
Microscopy of Fungi
Direct visual examination of:
Colorless, branching hyphae:
45’ branching septate hyphae:
Pseudohyphae with budding yeast:
Yeast with capsule halos and unequal budding:
Stains chitin in cell walls of fungi:
Cryptococcus neoformans:
Dimorphic fungi by incubation at 25C to identify hyphae,
followed by 37C to identify the yeast:
Fungi
Mold
Yeast
Dimorphic fungi
o Feces
o Blood
o Sputum
o Gastric lavage
Tinea
Aspergillus
Candida
Cryptococcus
Silver methenasmine
India ink
Sabouraud’s agar
o Urine
o Pus, CSF
Cryptococcosis
Fungal meningitis
Most common cause of:
Hodgkin’s disease, corticosteroid therapy, HIV infection
Predisposing factors:
Cryptococcus neoformans
Encapsulated budding yeast found in soil and dried pigeon
dung:
Inhalation
Route:
Signs/Symptoms:
*CNS disease predominates
o Headache
o Confusion
o Mental status changes
o Nuchal rigidity
o N/V
Lumbar puncture
Preferred diagnostic procedure:
Increase protein, decrease glucose, pleocytosis
Spinal fluid shows:
Budding encapsulated fungal cells
India ink or Gram stain shows:
Cryptococcal antigen CSF + establishes
To establish diagnosis:
Positive cryptoccal antigen
In HIV-infected pts CSF and serum shows:
Cryptococcal antigen
Sensitive screening test for meningitis:
Focal neurologic signs or papilledema- the test you use:
CT or MRI (r/o mass or hydrocephalus)
Amphotericin B IV followed by 8wks of Fluconazole PO
Treatment:
Flucytosine 100mg every 6hrs
Treatment- added early to prevent relapse:
1. Favorable clinical response
Switch to Fluconazole PO when:
2. Decrease antigen titer in CSF
3. Conversion of CSF culture to negative
Usual cause:
Areas colonized by this fungi:
Clinical illness results from:
Patients with preexisting asthma:
Treatment:
Complication in immunecompetent adults:
Most common in immunocompromised patients:
Mainstay of diagnosis:
Patchy infiltrates lead to:
Aspergillosis
Aspergillosis fumigates
Debris in the external auditory canal and burn eschar
Aberrant immune response or tissue invasion
Allergic bronchopulmonary aspergillosis
Prednisone- acute exacerbation
Itraconazole 200mg for 16weeks
Chronic sinusitis & aspergiloma (colonization of preexisting pulm. cavities)
Pulmonary disease
Tissue biopsy
Severe necrotizing pneumonia
As organism grows into blood vessel tissue:
Infarction occurs pleuritic chest pain and high serum LDH)
Blastomycosis
Cough, moderate fever, dyspnea, chest pain
Common symptoms:
Disseminated
Raised verrucous cutaneous lesions with abrupt downward
sloping borders:
When ribs and vertebrae is involved, radiographs show:
Destructive and proliferative lesions (labs not conclusive)
Itraconazole 100-200mg 2-3 months
Treatment:
Amphotericin
For treatment failures or CNS involvement:
Histoplasmosis:
Dimorphic fungi
Histoplasma capsulatum:
Bat or bird droppings in endemic areas
Isolated from soil contaminated with:
Asymptomatic
Most patients are:
Respiratory illness
Most common clinical manifestation:
Marked prostration, fever, and few respiratory complaints
Severe form of disease shows:
Progressive disseminated histoplasmosis
Usually fatal within 6wks or less:
o Ulcers of the
o Dyspnea, wt. loss o Cough, fever
Signs/symptoms:
oropharnynx
o prostration
o hepato/spleenomegaly
In pulmonary disease, sputum rarely:
Positive (unless chronic)
Blood C and S and bone barrow cultures are:
Positive (80%)
Treatment:
Treatment to prevent relapses:
Systemic mycosis due to inhalation of:
Symptoms:
2-20 days post symptoms patient may have:
Dissemination may occur in:
Serologic tests useful:
Suggestive lab finding:
In biopsied specimens, spherules filled with:
Treatment:
Meningeal coccidio requires :
Fluconazole is for:
Amphotericin B for post-op pts followed by:
To catch relapses:
Coccidiosis
Amphotericin B
Life-long suppressive therapy with ketoconazole or fluconazole
Coccidiomycosis
Arthroconidia of Coccidioides immitis
o Fever, chills
o Pleuritic pain
o Arthralgia
Erythema nodosum
Brain, bone, sin or soft tissue abscesses
Precipitin and immunodiffusion test (detect IgM antibodies)
Perisitent rising compliment fixation titer >1:16
Endospores
Amphotericin B
Intrathecal followed by an oral azole
Chest, bone and soft tissue
Azole
Serial complement fixation titers
Pneumocystosis
Pneumosystitis carinii
Isolated to mammal vectors:
o Cancer, HIV infx
o Severe malnutrition o Severe debility
Generally occurs in pts with:
Respiratory system
Usually limited to:
o Fever
o bibasilar crackles
o Nonproductive
Symptoms:
o tachypnea
o SOB
cough
Diagnosis depends on:
Morphological demonstration of the organisms (using specific stains)
Cultured
The organism can’t be:
To detect cysts, induced, lavaged or biopsied sputum stain w/: Giemsa stain or Methenamine Silver
Treatment:
Oral TMP-SMZ (low cost, high bioavailability)
Antibiotics
Pulmonary symptoms usually persit for 4-6 days after
initiation of:
Candida
Mucosal candidiasis
Esophageal involvement, most frequent type of invasive
disease:
Risk factors for invasive:
Prolonged neutropenia, recent surgery, broad-spectrum antibiotics,
intravascular catheters, and IVDA
Cellular immunodeficiency
HIV
Ris factors for mucocutaneous:
Persistent oral or vaginal candidiasis w/o underlying cause
suspect:
Esophageal Candidiasis (most frequent)
Substernal odynophagia, gastroesphogeal reflux or nausea without
substernal pain
Endoscopy with biopsy and culture
Fluconazole PO or amphotericin B IV
Symptoms:
Diagnosis is best confirmed by:
Treatment:
Vulvovaginal Candidiasis
Acute vulvar pruritis, burning discharge, dyspareunia
Clinical, culture
Clotrimazole 100mg x 7days or Fluconazole 150mg PO x 1
Symptoms:
Diagnosis:
Treatment:
Candidal Funguria
Indwelling catheter or antibiotics
Fluconazole 200mg x 7-14 days
Often resolves with discontinuation of:
Treatment:
Candidal fungemia
Fluffy white retinal infiltrates extending into vitreous
Amphotericin B
Flucytosine
Symptoms:
Treatment:
Treatment added if CNS involvement:
Candidal Endocaritis
Valvular cardiac surgery or IVDA
C albicans
Splenomegaly and petechia
Postivie cultures from emboli or valvular vegetation
Surgery and amphotericin B
Direct inoculation with:
Increased frequency on prosthetic valves within first few months:
Symptoms:
Diagnosis:
Treatment:
Body ringworm:
Jock itch:
Athletes foot:
Dermatophytosis
Pityriasis versicolor:
Diagnosis is directly showing fungi on:
If negative:
Treatment:
Good against dermatophytes and nail plate:
Superficial fungal infections
Tinea corporis
Tinea cruris
Tinea pedis
Tinea manuum
Tinea versicolor
10% HOG prep
Histological sections of nails stained with periodic acid-Schiff
Griseofulvin
terbinafine
HIV
+
Three CD4 T-lymphocyte categories
200-499:
Greater than or equal to 500:
Less than 200:
Applications of the CD4+ Count:
Category 2
Category 1
Category 3
1) Stages of HIV disease
2) Established the risk of specific HIV-associated complications
3) Determines the need for opportunistic infection prophylaxis
4) Assess response to anti-retroviral therapy
5) With viral load, determines the need for therapy
AIDS-defining illness or severe symptoms:
Asymptomatic w/CD4+ <200:
Treat
Treat
Asymptomatic w/CD4+between 200-350
Asymptomatic w/CD4+ T-cells >350 and plasma HIV RNA
>100,000:
Asymptomatic w/ CD4+ >350 and plasma<100,000:
Treatment offered w/ discussion of pros and cons
Defer therapy, some will treat
Defer therapy
Complications of HIV based on CD4+
>500 cells/mm:
<500 cells/mm:
<200 cells/mm:
< 100 cells/mm:
<50 cells/mm:
Category A:
Category B:
Category C:
o
o
o
o
o
o
Aids defining syndrome
A >10% loss of:
More than 30 days of:
Contributing factors:
Depression, oral ulcers, esophagitis, nausea, dementia:
GI infection:
Coexistent fever, diarrhea, malignancy, infection:
Appetite enhancers:
Anabolic steroids:
Nutrition:
HAART:
Neurological manifestations:
CNS lymphoma:
Neuropathy:
Progressive multifocal leukoencephalopathy:
Dermatological manifestations:
HIV (primary HIV infx, LAD, aseptic meningitis, ITP)
1. HSV (orogenital), VZV (shingles)
4. M. tuberculosis (pulm. TB)
2. Crypto Parvum (diarrhea)
5. Candida
3. Strep pneumo, H. flu
6. HHV-8 (Kaposi’s sarcoma)
Pneumocystis carinii (pneumonia) and crypto parvum
1. Toxoplasma gondii (encephalitis)
4. M. tuberculosis
2. Crypto neoformans (meningitis)
5. Microsporidia (diarrhea)
3. HSV, VZV, EBV
6. Candida (esophagitis)
3. Cytomegaloy virus
1. Mycobacterium avium
2. Aspergillosis sp.
4. HIV
Clinical manifestations
Documented HIV infection
o Primary HIV infection w/ illness
Asymptomatic HIV infection
o Persistent generalized LAD
Bacillary angiomatosis
o Candidiasis (Oro)
Hairy leukoplakia, oral
o Cervical dysplasia
Cadidiasis (bronchi, trachea, lungs)
o Candidiasis (esophageal)
Cryptosporidiosis (chronic
o HIV- associated dementia
intestinal)
o Kaposi’s sarcoma
Aids wasting syndrome
Lean body mass
Diarrhea, chronic weakness, fever
Decreased caloric intake
Decreased absorption
Increased metabolic demand/nutritional needs
Treatment
Marinol, megace
Testosterone, growth hormone
Oral supplementation, enteral, parenteral
Highly active anti-retroviral therapy
Dementia and toxoplasmosis
Non-hodgkin’s
Axonal sensorimotor peripheral neuropathy w/ varying patterns
JC polyoma virus
1. Herpes simplex
5. Herpes zoster
9. Kaposi’s sarcoma
2. Molluscum contagiousum
6. Bullous impetigo
10. Furuncles
3. Bacillary angiomatosis
7. Xerosis
11. Candida
4. Seborrheic dermatitis
8. Folliculitis
12. psoriasis
Lipodystrophy
Suspected to be caused by underlying HIV infx;
fat atrophy in face, extremities, and abdomen:
HIV/AIDS and Mycobacterium Tuberculosis
HIV infection
Single most important risk factor for TB:
Extrapulmonary or disseminated disease
Those with more advanced immunosuppression
are more likely to have:
HIV-uninfected presentation
CD4+ T lymphocyte count >350:
+
Extrapulmonary TB, high fevers, sepsis syndrome
CD4 T lymphocyte count <50:
Treatment of opportunistic infections and antiretroviral therapy
1. Reduce the incidence of opportunistic infections
Use of antiretroviral therapy has been shown to:
2. Improve survival in the setting of opportunistic infections
3. Reduces overall mortality among persons w/ HIV-1 infection
The greatest benefit is seen in HIV infected
patients with CD4+ T lymphocyte counts:
<200
Treatment of Specific Opportunistic Infection
Bactrim
ART
PO Famciclovir, Valacyclovir, and Acyclovir
PO Famciclovir, Valacyclovir, and Acyclovir
P. carinii pneumonia :
Kaposi’s sarcoma:
HSV (orolabial):
VSV (mild):
Toxoplasmosis
CMV Retinitis:
HPV:
Candidiasis:
Hepatitis C:
Sulfadiazine + Pyrimethamine w/leucovrin (prevents bone marrow loss)
Ganciclovir Intraocular implant + PO Valganciclover
Liquid nitrogen cryotherapy, Tricholoracetic or Bichloroacetic acid
topical Cidofovir, Podophyllin resin
PO fluconazole, bystatin, itraconazole oral solution
Interferon alfa or pegylated interferon
Hepatitis B
M. Avium complex:
Interferon alfa, lamivudine + adefovir or tenofovir
Clarirthromycin or Axithromycin + Ethambutol and Rifabutin
Immune reconstitution Syndrome
Potent anti-retroviral therapy
Atypical or unusual local inflammatory manifestation of opportunistic infx
Cytomegalovirus retinitis development into vitreitis
M. avium complex focal lymphadenitis or granuloma mass formation
Paradoxical reactivation or worsening of M. tuberculosis
Continue ART, low dose steroids
Treatment:
+
MMR may be given if asymptomatic and CD4 T- 200
lymphocyte greater than:
Occurs following the initiation of:
Characterized by:
Examples:
Known as:
Acute infection of:
Caused by:
Highly contagious transmission through:
Highest incidence in:
It was a leading cause of:
Pertussis
Whooping cough
Respiratory tract
Bordtella pertussis
Airborne droplets
Summer and fall
Child mortality
Pathophysiology- Bordatella Pertussis (small aerobic gram negative rod)
Pertussis toxin
Histamine sensitization and lymphcytosis
Tracheal cytotoxin ,dermonecrotic factor, adenylate cyclase
Local epithelial damage (produces resp symptoms, leads to absorption of
Pertussis toxin)
Host defenses (along w/adenylate cyclase toxin)
Attach to respiratory cilia via:
Pertussis toxin leads to:
Produces virulence factors including:
Virulence factors are responsible for:
Pertussis toxin impairs:
Clinical Features
Insidious onset of coryza, sneezing, low-grade fever, mild cough:
Paroxysms of numerous, rapid coughs
At the end of the paroxysm, a long inspiratory effort is usually
accompanied by a characteristic:
Recovery; coughing spells les frequent:
Pertussis in adults:
Source of infection for children:
The gold standard diagnosis is:
Rapid, sensitive, specific, amplifies DNA sequence; in addition
to culture:
Testing of nasopharyngeal specimens if symptomatic >4wks:
Eradicates organism from secretions; 14 days:
Prophylaxis for all household contacts:
Catarrhal stage (over 2wks cough becomes more severe)
Paroxysmal stage(more frequently at night)
High-pitched whoop (most contagious)
Convalescence stage
Mild course, no inspiratory whoop
Adults
Nasopharyngeal culture (placed on bordet-gengou medium)
PCR
Direct Fluorescent Antibody (low sensitivity and specificity)
Erythromycin
Trimethroprim- Sulfamethoxazole (Bactrim)
Inactivated B. Pertussis cells (Formalin)
Purified inactivated B. pertussis (more effective)
Diphtheria, tetanus, pertussis
Infanrix
tripedia
Whole cell pertussis vaccine:
Acellular pertussis vaccine:
DTaP:
3 antigens mostly pertussis toxin, and FHA:
FHA and PT:
Toxic Shock Syndrome
Exotoxin
Staphylococcus aureus or group A beta-hemolytic strep
The immune system
Due to:
Produced by:
This toxin is a superantigen that can stimulate:
Staphylococcus aureus- pathophysiology
Endotoxin toxin-1
Tampon use in young women
Due to:
Many associated with:
Streptococci- pathophysiology
Triggered by:
Produce:
Strep enters the body through:
Invades deeper soft tissue producing:
Clinical presentation- staphylococcus aureus:
Clinical presentation- GAS:
Diagnosis of toxic shock syndrome:
Diagnosis of group A strep:
Treatment:
Certain group A streptococcal bacteria (GAS)
Exotoxin A and S pyogenes exotoxin B
Open wound or bruise
Destructive soft tissue infection (myositis, fasciitis)
Diffuse erythematous rash w/ desquamation on hands and feet
Redness to eyes w/out purulent discharge
N/V/D, high fever/chills, malaise, pharyngitis, h/a, myalgia
Signs of soft tissue infection, bullae, desquamation, petechaie
Fever, muscle aches, confusion
Fever, low blood pressure, rash, 3 organs w/ dysfunction
Hypoalbuminemia, hypotension, hypocalcemia, elevated liver enzymes,
prolonged PT/PTT, elevated creatine level/BUN
Fluid resuscitation, oxygen, penicillinase-resistant antibiotics
(Clindamycin or Vancomycin, Nafcillin), incision/drainage
HIV testing: pre and post counseling
1. Access to testing
Ensure patients infected and those at risk for infection have:
2. Receive HIV prevention counseling
3. Access to medical and psychological support
At Risk groups for HIV
Behavioral risk:
Clinical signs and symptoms:
Seeks to reduce HIV acquisition and transmission by providing:
HIV prevention counseling:
Used when immediate results necessary:
Most HIV in US are:
Standard Testing Algorithm- initial screening with:
Western blot looks for:
If EIA is positive then:
Induced antibodies may be detected by tests and give false
positive from:
Health care providers must report all newly diagnosed cases of
HIV infection to:
Post exposure prophylaxis should begin within:
Post exposure prophylaxis includes:
Most infected persons develop antibodies within:
IV drug use, unprotected intercourse
clinical manifestations of acute retroviral or opportunistic
infections
HIV transmission and prevention and explanation of HIV test
results, and referral information
identifies behaviors putting patient at risk for HIV
Rapid testing
HIV-1 group B
Enzyme immunoassay antibodies (EIA) to viral proteins
Viral bands (p24, gp41, gp120/160)
Retest twice
HIV vaccine
NYS DOH
72 hours of exposure
Zidovudine, Lamivudine or Zidovudine and emtricitabine daily for
4 weeks
3 months of exposure