Candida

Candida

dmid

dmid

Thymus histology
Spleen histology
Lymph node histology
Introduction to the immune system
Cytokines
Innate immune system
Complement system
T-cell development
B-cell development
MHC class I and MHC class II molecules
T-cell activation
B-cell activation, differentiation, and contraction
Cell-mediated immunity of CD4 cells
Cell-mediated immunity of natural killer and CD8 cells
Antibody classes
Somatic hypermutation and affinity maturation
VDJ rearrangement
Contracting the immune response and peripheral tolerance
B- and T-cell memory
Anergy, exhaustion, and clonal deletion
Vaccinations
Type I hypersensitivity
Type II hypersensitivity
Type III hypersensitivity
Type IV hypersensitivity
Sepsis
Neonatal sepsis
Abscesses
Food allergy
Anaphylaxis
Asthma
Immune thrombocytopenia
Autoimmune hemolytic anemia
Hemolytic disease of the newborn
Rheumatic heart disease
Myasthenia gravis
Graves disease
Pemphigus vulgaris
Serum sickness
Systemic lupus erythematosus
Poststreptococcal glomerulonephritis
Graft-versus-host disease
Contact dermatitis
Transplant rejection
Cytomegalovirus infection after transplant (NORD)
Post-transplant lymphoproliferative disorders (NORD)
X-linked agammaglobulinemia
Selective immunoglobulin A deficiency
Common variable immunodeficiency
IgG subclass deficiency
Hyperimmunoglobulin E syndrome
Isolated primary immunoglobulin M deficiency
Thymic aplasia
DiGeorge syndrome
Severe combined immunodeficiency
Adenosine deaminase deficiency
Ataxia-telangiectasia
Hyper IgM syndrome
Wiskott-Aldrich syndrome
Leukocyte adhesion deficiency
Chediak-Higashi syndrome
Chronic granulomatous disease
Complement deficiency
Hereditary angioedema
Asplenia
Thymoma
Ruptured spleen
Immunodeficiencies: T-cell and B-cell disorders: Pathology review
Immunodeficiencies: Combined T-cell and B-cell disorders: Pathology review
Immunodeficiencies: Phagocyte and complement dysfunction: Pathology review
Glucocorticoids
Bacterial structure and functions
Staphylococcus epidermidis
Staphylococcus aureus
Staphylococcus saprophyticus
Streptococcus viridans
Streptococcus pneumoniae
Streptococcus pyogenes (Group A Strep)
Streptococcus agalactiae (Group B Strep)
Enterococcus
Clostridium perfringens
Clostridium botulinum (Botulism)
Clostridium difficile (Pseudomembranous colitis)
Clostridium tetani (Tetanus)
Bacillus cereus (Food poisoning)
Listeria monocytogenes
Corynebacterium diphtheriae (Diphtheria)
Bacillus anthracis (Anthrax)
Nocardia
Actinomyces israelii
Escherichia coli
Salmonella (non-typhoidal)
Salmonella typhi (typhoid fever)
Pseudomonas aeruginosa
Enterobacter
Klebsiella pneumoniae
Shigella
Proteus mirabilis
Yersinia enterocolitica
Legionella pneumophila (Legionnaires disease and Pontiac fever)
Serratia marcescens
Bacteroides fragilis
Yersinia pestis (Plague)
Vibrio cholerae (Cholera)
Helicobacter pylori
Campylobacter jejuni
Neisseria meningitidis
Neisseria gonorrhoeae
Moraxella catarrhalis
Francisella tularensis (Tularemia)
Bordetella pertussis (Whooping cough)
Brucella
Haemophilus influenzae
Haemophilus ducreyi (Chancroid)
Pasteurella multocida
Mycobacterium tuberculosis (Tuberculosis)
Mycobacterium leprae
Mycobacterium avium complex (NORD)
Mycoplasma pneumoniae
Chlamydia pneumoniae
Chlamydia trachomatis
Borrelia burgdorferi (Lyme disease)
Borrelia species (Relapsing fever)
Leptospira
Treponema pallidum (Syphilis)
Rickettsia rickettsii (Rocky Mountain spotted fever) and other Rickettsia species
Coxiella burnetii (Q fever)
Ehrlichia and Anaplasma
Gardnerella vaginalis (Bacterial vaginosis)
Viral structure and functions
Varicella zoster virus
Cytomegalovirus
Epstein-Barr virus (Infectious mononucleosis)
Human herpesvirus 8 (Kaposi sarcoma)
Herpes simplex virus
Human herpesvirus 6 (Roseola)
Adenovirus
Parvovirus B19
Human papillomavirus
Poxvirus (Smallpox and Molluscum contagiosum)
BK virus (Hemorrhagic cystitis)
JC virus (Progressive multifocal leukoencephalopathy)
Poliovirus
Coxsackievirus
Rhinovirus
Hepatitis A and Hepatitis E virus
Hepatitis D virus
Influenza virus
Mumps virus
Measles virus
Respiratory syncytial virus
Human parainfluenza viruses
Dengue virus
Yellow fever virus
Zika virus
Hepatitis C virus
West Nile virus
Norovirus
Rotavirus
Coronaviruses
HIV (AIDS)
Human T-lymphotropic virus
Ebola virus
Rabies virus
Rubella virus
Eastern and Western equine encephalitis virus
Lymphocytic choriomeningitis virus
Hantavirus
Prions (Spongiform encephalopathy)
Coccidioidomycosis and paracoccidioidomycosis
Histoplasmosis
Blastomycosis
Pneumocystis jirovecii (Pneumocystis pneumonia)
Candida
Mucormycosis
Aspergillus fumigatus
Sporothrix schenckii
Cryptococcus neoformans
Malassezia (Tinea versicolor and Seborrhoeic dermatitis)
Plasmodium species (Malaria)
Babesia
Giardia lamblia
Entamoeba histolytica (Amebiasis)
Cryptosporidium
Acanthamoeba
Naegleria fowleri (Primary amebic meningoencephalitis)
Toxoplasma gondii (Toxoplasmosis)
Trypanosoma brucei
Trypanosoma cruzi (Chagas disease)
Trichomonas vaginalis
Leishmania
Loa loa (Eye worm)
Toxocara canis (Visceral larva migrans)
Onchocerca volvulus (River blindness)
Ascaris lumbricoides
Anisakis
Angiostrongylus (Eosinophilic meningitis)
Ancylostoma duodenale and Necator americanus
Strongyloides stercoralis
Guinea worm (Dracunculiasis)
Wuchereria bancrofti (Lymphatic filariasis)
Trichinella spiralis
Enterobius vermicularis (Pinworm)
Trichuris trichiura (Whipworm)
Echinococcus granulosus (Hydatid disease)
Diphyllobothrium latum
Paragonimus westermani
Clonorchis sinensis
Schistosomes
Pediculus humanus and Phthirus pubis (Lice)
Sarcoptes scabiei (Scabies)
Protein synthesis inhibitors: Aminoglycosides
Antimetabolites: Sulfonamides and trimethoprim
Antituberculosis medications
Miscellaneous cell wall synthesis inhibitors
Protein synthesis inhibitors: Tetracyclines
Cell wall synthesis inhibitors: Penicillins
Miscellaneous protein synthesis inhibitors
Cell wall synthesis inhibitors: Cephalosporins
DNA synthesis inhibitors: Metronidazole
DNA synthesis inhibitors: Fluoroquinolones
Mechanisms of antibiotic resistance
Integrase and entry inhibitors
Nucleoside reverse transcriptase inhibitors (NRTIs)
Protease inhibitors
Hepatitis medications
Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
Neuraminidase inhibitors
Herpesvirus medications
Azoles
Echinocandins
Miscellaneous antifungal medications
Anthelmintic medications
Antimalarials
Anti-mite and louse medications
Advanced cardiac life support (ACLS): Clinical
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Coronary artery disease: Clinical
Heart failure: Clinical
Syncope: Clinical
Pericardial disease: Clinical
Valvular heart disease: Clinical
Chest trauma: Clinical
Shock: Clinical
Peripheral vascular disease: Clinical
Leg ulcers: Clinical
Aortic aneurysms and dissections: Clinical
Cholinomimetics: Direct agonists
Cholinomimetics: Indirect agonists (anticholinesterases)
Muscarinic antagonists
Sympathomimetics: Direct agonists
Sympatholytics: Alpha-2 agonists
Adrenergic antagonists: Presynaptic
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
ACE inhibitors, ARBs and direct renin inhibitors
Loop diuretics
Thiazide and thiazide-like diuretics
Calcium channel blockers
cGMP mediated smooth muscle vasodilators
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Positive inotropic medications
Antiplatelet medications
Blistering skin disorders: Clinical
Bites and stings: Clinical
Burns: Clinical
Diabetes mellitus: Clinical
Hyperthyroidism: Clinical
Hypothyroidism and thyroiditis: Clinical
Parathyroid conditions and calcium imbalance: Clinical
Adrenal insufficiency: Clinical
Neck trauma: Clinical
Insulins
Mineralocorticoids and mineralocorticoid antagonists
Abdominal pain: Clinical
Appendicitis: Clinical
Gastrointestinal bleeding: Clinical
Peptic ulcers and stomach cancer: Clinical
Inflammatory bowel disease: Clinical
Diverticular disease: Clinical
Gallbladder disorders: Clinical
Pancreatitis: Clinical
Cirrhosis: Clinical
Hernias: Clinical
Bowel obstruction: Clinical
Abdominal trauma: Clinical
Laxatives and cathartics
Antidiarrheals
Acid reducing medications
Blood products and transfusion: Clinical
Venous thromboembolism: Clinical
Anticoagulants: Heparin
Anticoagulants: Warfarin
Anticoagulants: Direct factor inhibitors
Thrombolytics
Fever of unknown origin: Clinical
Infective endocarditis: Clinical
Pneumonia: Clinical
Tuberculosis: Pathology review
Diarrhea: Clinical
Urinary tract infections: Clinical
Meningitis, encephalitis and brain abscesses: Clinical
Skin and soft tissue infections: Clinical
Hypernatremia: Clinical
Hyponatremia: Clinical
Hyperkalemia: Clinical
Hypokalemia: Clinical
Metabolic and respiratory acidosis: Clinical
Metabolic and respiratory alkalosis: Clinical
Toxidromes: Clinical
Medication overdoses and toxicities: Pathology review
Environmental and chemical toxicities: Pathology review
Acute kidney injury: Clinical
Kidney stones: Clinical
Stroke: Clinical
Seizures: Clinical
Headaches: Clinical
Traumatic brain injury: Clinical
Lower back pain: Clinical
Spinal cord disorders: Pathology review
Anticonvulsants and anxiolytics: Barbiturates
Anticonvulsants and anxiolytics: Benzodiazepines
Nonbenzodiazepine anticonvulsants
Migraine medications
Osmotic diuretics
Opioid agonists, mixed agonist-antagonists and partial agonists
Opioid antagonists
Asthma: Clinical
Chronic obstructive pulmonary disease (COPD): Clinical
Acute respiratory distress syndrome: Clinical
Pleural effusion: Clinical
Pneumothorax: Clinical
Bronchodilators: Beta 2-agonists and muscarinic antagonists
Pulmonary corticosteroids and mast cell inhibitors
Joint pain: Clinical
Anatomy clinical correlates: Clavicle and shoulder
Anatomy clinical correlates: Axilla
Anatomy clinical correlates: Arm, elbow and forearm
Anatomy clinical correlates: Wrist and hand
Anatomy clinical correlates: Median, ulnar and radial nerves
Anatomy clinical correlates: Bones, joints and muscles of the back
Acetaminophen (Paracetamol)
Non-steroidal anti-inflammatory drugs
Antigout medications
Pediatric allergies: Clinical
Kawasaki disease: Clinical
Congenital TORCH infections: Pathology review
Pediatric infectious rashes: Clinical
Pediatric bone and joint infections: Clinical
Sjogren syndrome: Clinical
Vasculitis: Clinical
Rheumatoid arthritis: Clinical
Seronegative arthritis: Clinical
Systemic lupus erythematosus (SLE): Clinical
Inflammatory myopathies: Clinical
ECG axis
ECG basics
Normal heart sounds
Abnormal heart sounds
Cardiac conduction system
Cardiac conduction velocity
ECG normal sinus rhythm
ECG intervals
ECG QRS transition
ECG rate and rhythm
ECG cardiac infarction and ischemia
ECG cardiac hypertrophy and enlargement
Vasculitis

Transcript

Watch video only

Candida is a yeast, not the maple syrup-loving country in North America - although Candida can be found in Canada as well!

Candida sometimes causes a mild yeast infection, but in some situations, can get into the bloodstream and cause severe illness.

Now, there are various types of Candida species, and over twenty of them cause disease in humans - C. albicans, C. parapsilosis, C. tropicalis, C. glabrata, C. krusei, C. auris, the list goes on.

Of these, the most common one is C. albicans. Candida is found throughout the body; it likes warm, moist environments like the mouth, the diaper region of babies, and in women it can be found in the vagina.

Now, it’s normal for microbes - bacteria, fungi, and viruses - to live all over the body, but each microbe is slightly different in terms of whether it’s colonizing the body - in other words just living and not causing any problems, or whether it’s infecting the body, causing some degree of tissue damage or destruction.

An important factor is exactly how much of a microbe is present.

Candida is considered an opportunistic microbe.

When the amount of Candida is relatively low, it's harmless.

But if a person’s immune system is weakened or if there’s less competition for the Candida, then the amount of Candida can increase - and that’s called Candida overgrowth.

Now, Candida can exist in multiple forms - it’s a bit like a chameleon.

Sometimes the cells can appear round or oval and these are called yeast cells, other times it can appear like hyphae where it looks like long thin filaments - kind of like a segmented cactus plant.

It can also take an in-between appearance called pseudohyphae.

Each of these morphologies or “looks” reflect the same Candida cells that are expressing different protein profiles, and they give the cells different properties.

When the Candida is in “yeast mode” it’s better at moving from one part of the body to another, whereas when it’s in “filamentous mode” it’s better at invading tissues.

Candida typically lives on the skin or mucous membranes, and when it starts to overgrow it can damage nearby tissue.

There are a few patterns of injury, the most common one is pseudomembranous candidiasis, and it’s primarily due to a weakened immune system that allows for Candida overgrowth.

The result is destruction of the stratified squamous epithelium layer, which is the outermost layer of the skin or mucous membranes.

This causes accumulation of the destroyed cells and the keratin protein that fills that outermost layer, forming a white lesion, called a pseudomembrane, that looks kind of like “cottage cheese”.

The white lesions aren’t typically painful and they can be scraped away with a tongue depressor, leaving behind a red mucosal base which sometimes bleeds.

Since the underlying cause is a weakened immune system, it’s fairly common in young infants and the elderly, both groups that have a relatively weak immune system.

It can also be related to an immunosuppressive condition like diabetes or HIV, or from immunosuppressive medical treatments like steroids - including inhaled steroids, as well as radiotherapy or chemotherapy.

Another pattern of injury is called erythematous candidiasis and that typically results from a change in the levels of microbial competition keeping Candida in check.

For example, a course of antibiotics or tobacco smoking, which both selectively destroy certain bacterial populations more than they affect Candida.

The opposite is true as well, sometimes there are mechanical devices like braces that favor Candida growth more than the growth of other microbes.

In either situation, the result is an overgrowth of Candida which causes increased blood flow to the affected tissue with red painful lesions.

In a lot of situations there’s a mixed pattern of injury with both a pseudomembranous and erythematous component.