I Made This Because I Can Never Get It Right! Hope This Helps Others. 

This one’s about bugs

Guys, I love ID. I really hope I get to do an ID rotation on Medicine. If you remember, I once posted the mnemonic I swear by for viruses. Well here is the bacteria counterpart. Also your micro mantra should be: sketchy is life. Love Andrew like I do (this part’s not the mantra, I just love Andrew).

Let me know if you have any questions or need clarification. This is a perfect example of a “not aesthetically pleasing tumblr study post” because sometimes your handwriting sucks and you aint got that kinda time in my life for pretty arrows and banners and I just wanna finish this shit so I can leave the library when will Step 1 even be over why is this my liiiiiife

If you cannot grasp what I have just explained, you should just leave and study economics!

Microbiology professor, first lecture (via scienceprofessorquotes)

Influenza

Happy flu season! I’ve just been stuck inside for 5 days with a mild case, so this is a bit bitter

There are 3–5 million cases of flu per year, and ~375,000 deaths, usually in older, younger, and immunocompromised individuals.

Enveloped, Single-stranded RNA virus

First identified in 1933, but existed long before

Generally considered an infection of the bronchi

so effectively a form of bronchitis – i.e. it causes inflammation of the bronchi 

There are 3 types - A, B and C

B & C appear restricted to humans 

C is less common

A is found in wide range of species including pigs and poultry as well as man

Type A appears to be responsible for more severe disease

Basics

Transmission by aerosols

Incubation ~2 days

Contagious during first 3-5days of illness

Symptoms – fever, myalgia, headache, dry cough, sore throat, aches, fatigue

Recovery ~7-10 days for most

Complications – most frequent = secondary bacterial pneumonia, rarely = viral pneumonia, myocarditis, encephalitis

No specific treatment

Vaccination for high risk groups including the elderly, health care workers, those with underlying respiratory conditions.

Avian

The main reservoir is wildfowl that are resistant to the disease

doesn’t usually affect animals other than poultry and pigs

However some transfer events occur

Seasonal

Incidence highest in winter

Strains vary from year to year -  hard to predict and vaccinate (this year’s vaccine has been pretty rubbish)

Pandemic

Can be caused by any strain that has not been seen in the human population for many years

New strains evade the herd immunity that exists to previously encountered strains

1918 /19 –( Spanish) estimated 40-50 million deaths worldwide

1957 – Influenza A/H1N1 (Asian)

1968 – Influenza A/H3N2 (Hong Kong)

Eventually the virus runs out of susceptible hosts and the epidemic fizzles out

Experts generally agree another pandemic is inevitable, and may be imminent – maybe we have had some minor pandemics 

16000 confirmed H1N1 deaths in 2009 affecting over 200 countries

Consensus is that the prompt action of the Hong Kong authorities probably prevented a pandemic in 1997

The prediction is scary - for industrialised countries they predic 1.0 – 2.3 million hospitalisations

280,000-650,000 deaths 

in two years

A network of 112 centres monitor flu isolates to identify unusual strains that can then be examined further

The WHO has a Pandemic Preparedness Plan in place http://www.who.int/influenza/preparedness/pandemic/en/

Diagnosis

Generally based on GP diagnosis

Virus isolation / virus demonstration from nasopharyngeal secretions during acute phase

Demonstration of viral antigen in secretions

Antibody rise using paired sera ( 1st sample taken between days 1-3 of illness, 2nd taken around day 12 of illness) by haemagglutination inhibition or complement fixation test

Molecular methods evolving rapidly – in particular in response to the recent epidemic/pandemic strains emerging

A range of respiratory illnesses have the same symptoms, only laboratory testing can confirm the aetiological agent

Treatment/Vaccination 

In the UK NICE argue that immunisation against predicted strains is the best form of defence – traditionally focused on the elderly and those with underlying lung problems, but recently started rolling out a childhood vaccine (nasal spray)

Vaccines generally based on the H & N surface structures which mutate, however hopes of an M protein based vaccine which will give longer lasting protection raised recently

Antivirals

Antivirals not recommended in otherwise healthy people (amantadine should not be used at all) - should ride it out

However when incidence reaches a certain level zanamivir and oseltamivir should be used in those considered high risk for the development of complications – PROVIDED THAT TREATMENT IS STARTED WITHIN 48 HOURS OF ONSET OF SYMPTOMS

Resistance is becoming an issue

Clostridium botulinum

Gram+, anaerobe, spore forming, motile rods

Botulin toxin (botox) inhibits the release of ACh and produces a flacid paralysis.

Adults ingest the toxin from poorly heated canned food (labile toxin, 60° 10minutes): weakness, diplopia, flacid paralysis and respiratory muscles involved, vomiting, diarrhea.

Infants ingest the spore from the dust or honey and form the toxins in the gut: constipation, weak crying, weak feeding, flacid paralysis and rapid respiratory involvement

Wound: traumatic implantation (assoc. w/ IVDA; uncommon), same symptoms without GI symptoms. Debridement, no closure.

Organophosphate poisoning VS Atropine poisoning

Innate Immunity - intro

First line of defence + first to act

A primitive response (exists in animals and some plants)

Non-specialised and without ‘memory’

Consists of:

Physical barriers (eg skin and mucosa//tight junctions, airflow)

Chemical barriers (eg enzymes, lung surfactant, antimicrobals)

Soluble mediators of inflammation (eg cytokines)

Microbal defence (eg commensal competition, secreted antimicrobals)

Cells (eg phagocytes)

Receptors to recognise presence of pathogen/injury - results in inflammation

Soluble Mediators

Complement Proteins

liver-derived 

circulate in serum in inactive form

activated by pathogens during innate response

functions include lysis, chemotaxis and opsonisation

Auxiliary Cells

Mediate inflammation as part of the immune response. The main auxiliary cells involved in the immune response are Basophils, Mast cells and Platelets.

Basophils 

Leukocyte containing granules 

on degranulation release histamine + platelet activating factor

causing increased vascular permeability and smooth muscle contraction

also synthesise and secrete other mediators that control the development of immune system reactions

Mast Cells

Also contain granules 

However they are not circulating cells - found close to blood vessels in all types of tissue especially mucosal and epithelial tissues.

rapidly release inflammatory histamine but this is IgE dependant so not innate

Platelets 

normally function in blood clotting

also release inflammatory mediators

Cytokines and chemokines

Produced by many cells but especially mØ (macrophages), initiate inflammatory response and act on blood vessels 

interferons - antiviral protection

chemokines - recruit cells

interleukines - fever inducing, IL-6 induces acute phase proteins 

IL-1 - encourages leukocytes to migrate to infected/damaged tissue

as does tumour necrosis factor (TNFa)

Acute phase proteins

Liver derived proteins 

plasma concentrations increase (positive acute-phase proteins) or decrease (negative acute-phase proteins) in response to inflammation

called the acute-phase reaction 

triggered by inflammatory cytokines ( IL-1, IL-6, TNFα)

help mediate inflammation ( fever, leukocytosis, increased cortisol, decreased thyroxine, decreased serum iron, etc)

activate complement opsonisation 

Inflammation 

Cells

Cytotoxic Cells

Eosinophils/natural killer cells, cytotoxic T cells

kill target via release of toxic granules 

dendritic cell derived IL-12 helps activate NK cells

Phagocytes

mono-nuclear = long-lived; polynuclear = short-lived

engulf, internalize and destroy 

phagosome forms around microbe

enzyme filled with lysosomes fuses to form phagolysosome

organism is digested

fragments are either ‘presented’ or exocytosed

phagocytosis requires recognition of microbe via receptors for

PAMPs (pathogen associated molecular patterns - eg flagella or capsule) - recognised by toll-like receptors 

activated complement

antibody

The innate immune response primes for the adaptive 

B-cells are primed by activated complement

Th1 cell differentiation needs pro-inflammatory cytokines

Gram Negative Aerobic Rods Mnemonic

MICROBIOLOGY MNEMONIC 

BRUno, FRANCISco & COnstantine are BORing PSEUDO LEGIONnaires

Brucella sp 

Francisella tularensis 

Coxiella burnetti

Bortedella pertusis

Pseudomona aeuroginosa

Legionella pneumophila

Sketchy Micro To Do List: 

• 01 - Gram Positive Cocci o 1.1 - Staph Aureus (11:03) o 1.2 - Staph Epidermidis (6:54) o 1.3 - Strep pyogenes (Group A Strep) (14:30) o 1.4 - Strep agalactiae (Group B Strep) (5:23) o 1.5 - Strep. pneumoniae Strep viridans (9:17) o 1.6 - Enterococcus (4:06) • 02 - Gram Positive Bacilli o 2.1 - Bacillus anthracis and Bacillus cereus (9:50) o 2.2 - Clostridium tetani (6:42) o 2.3 - Clostridium botulinum (7:35) o 2.4 - Clostridium difficile (8:17) o 2.5 - Clostridium perfringens (5:31) o 2.6 - Corynebacterium diphtheriae (6:49) o 2.7 - Listeria monocytonegenes (4:04) • 03 - Gram-Positive Branching Filamentous Rods o 3.1 - Actinomyces (3:01) o 3.2 - Nocardia (6:50) • 04 - Gram-Negative Cocci o 4.1 - Neisseria species overview (5:07) o 4.2 - Neisseria meningitidis (8:59) o 4.3 - Neisseria gonorrheae (7:33) • 05 - Gram-Negative Bacilli - Enteric tract o 5.1 - Klebsiella, Enterobacter, Serratia (7:49) o 5.10 - Proteus mirabilis (2:54) o 5.2 - Salmonella (5:51) o 5.3 - Shigella (6:26) o 5.4 - Escherichia coli (ETEC, EHEC) (8:51) o 5.5 - Yersinia enterocolitica (7:54) o 5.6 - Campylobacter (5:30) o 5.7 - Vibrio (5:45) o 5.8 - Helicobacter (5:23) o 5.9 - Pseudomonas (9:59) • 06 - Gram-Negative Bacilli - Respiratory tract o 6.1 - Bordatella pertussis (7:39) o 6.2 - Haemophilus influenzae (8:46) o 6.3 - Legionella (7:26)

• 07 - Gram-Negative Bacilli - Zoonotics o 7.1 - Bartonella henselae (4:15) o 7.2 - Brucella (4:41) o 7.3 - Francisella tularensis (3:50) o 7.4 - Pasteurella multocida (3:55) • 08 - Mycobacteria o 8.1 - Mycobacterium tuberculosis (16:35) o 8.2 - Mycobacterium leprae (9:17) • 09 - Spirochetes o 9.1 - Borrelia (8:16) o 9.2 - Leptospirosis (4:18) o 9.3 - Treponema Pallidum (12:52) • 10 - Gram-Indeterminate Bacteria o 10.1 - Chlamydia (15:08) o 10.2 - Coxiella burnetii (4:57) o 10.3 - Gardnerella vaginalis (5:32) o 10.4 - Mycoplasma pneumoniae (5:57) o 10.5 - Rickettsia species overview (3:34) o 10.6 - Rickettsia prowazekii (4:11) o 10.7 - Rickettsia rickettsii (4:00) • Fungi • 1 - Systemic Mycoses o 1.1 - Histoplasmosis (9:38) o 1.2 - Blastomycosis (6:09) o 1.3 - Coccidioidomycosis (7:26) o 1.4 - Paracoccidioidomycosis (4:55) • 2 - Cutaneous Mycoses o 2.1 - Malassezia furfur :0Pityriasis Versicolor (5:10) o 2.2 - Dermatophytes (6:01) o 2.3 - Sporothrix schenckii (4:24) • 3 - Opportunistic Fungal Infections o 3.1 - Candida albicans (12:49) o 3.2 - Aspergillus fumigatus (10:51) o 3.3 - Cryptococcus neoformans (9:00) o 3.4 - Mucormycosis (6:17) o 3.5 - Pneumocystis pneumonia (5:49)

• Parasites • 1 - Protozoa of the Intestinal Tract o 1.1 - Giardia (5:19) o 1.2 - Entamoeba histolytica (7:55) o 1.3 - Cryptosporidium (4:31) • 2 - Protozoa of the CNS o 2.1 - Toxoplasmosis (10:21) o 2.2 - Trypanosoma brucei (4:45) o 2.3 - Naegleria fowleri (6:01) • 3 - Protozoa of the Blood o 3.1 - Trypanosoma cruzi (5:43) o 3.2 - Babesia (6:59) o 3.3 - Plasmodium species (13:57) o 3.4 - Leishmaniasis (5:47) • 4 - Protozoa - Other Tissue o 4.1 - Trichomoniasis (5:37) • 5 - Helminths - Nematodes o 5.1 - Intestinal nematodes (13:09) o 5.2 - Tissue Nematodes (11:29) • 6 - Helminths - Trematodes and Cestodes o 6.1 - Cestodes (10:20) o 6.2 - Trematodes (10:56)

• Viruses • 1 - RNA Viruses - Positive Sense o 1.1 - Picornavirus Overview (10:47) o 1.2 - (Pico) Poliovirus (7:18) o 1.3 - (Pico) Coxsackievirus (5:10) o 1.4 - (Pico) Rhinovirus (4:45) o 1.5 - (Pico) Hepatitis A (7:00) o 1.6 - (Norwalk) Calicivirus (5:26) o 1.7 - Flavivirus (8:16) o 1.8 - Hepatitis C Virus (10:24) o 1.9 - Togavirus (11:20) o 1.10 - Coronavirus (3:32) o 1.11 - HIV (16:24) • 2 - RNA Viruses - Negative Sense o 2.1 - Orthomyxovirus (18:23) o 2.2 - Paramyxovirus (15:57) o 2.3 - Rhabdovirus (9:02) o 2.4 - Filovirus (4:54) o 2.5 - Bunyavirus (5:41) o 2.6 - Arenavirus (5:15) o 2.7 - Reovirus (7:15) • 3 - DNA Viruses o 3.1 - HSV-1 and HSV-2 (11:15) o 3.10 - Adenovirus (4:52) o 3.11 - Poxvirus (8:26) o 3.12 - Hepatitis B Virus (18:38) o 3.2 - EBV (13:24) o 3.3 - CMV (11:51) o 3.4 - VZV (11:45) o 3.5 - HHV-6 (5:12) o 3.6 - HHV-8 (7:10) o 3.7 - Polyomavirus JC & BK (6:31) o 3.8 - Papillomavirus (13:47) o 3.9 - Parvovirus (7:07)

CAMP test for the identification of Streptococcus agalactiae (group B). 

(A) Streptococcus (group B) shows a positive CAMP reaction arrow-shaped zone of enhanced hemolysis .

(B) Streptococcus pyogenes (group A) shows a negative reaction when inoculated at a right angle to

© Staphylococcus aureus.

CYSTIC FRIBROSIS

G511D mutation: missense mutation, Glycine replaced by Aspartate.

Only 5% of pts with CF have this mutation.

Defective channel opening or gating.

IVACAFTOR: new drug, acts directly in the CFTR channel, opens it up. First drug that afects the ethiology :)

Trade name: Kalydeco