BRS Microbiology and Immunology PDF FREE DOWNLOAD

Immune System OverviewHere we will learn about the immune system, which combats disease-causing organisms.Pathogens Disease-causing or harmful microorganismsAntigens Material that can evoke an immune response Innate Immune BranchNon-specific, fastThe innate branch is non-specific (it reacts to a broad range of microbes) and is fast (responses occur within hours of infection).Actors of the Innate SystemPhysical barriers: - Epidermal cells create a slightly acidic surface and release enzymes and other antimicrobial peptides that make the skin surface inhospitable to microbes.Chemical barriers: - Some body surfaces (such as the respiratory pathways) are also covered in mucus, which can trap microbes before they can infect the body.Chemokines: Chemical signal produced by damaged cell to alert the body to danger and act as a homing signal for immune cellsNeutrophils: First type of phagocytic cell to arriveMonocytes: Arrive and mature into macrophages which engulf and destroy pathogensInflammation: Response to tissue damage, four clinical signs: redness, heat, swelling and pain.Innate System in ActionPathogens gain entry to the inside of the body through the wound.Chemokine chemical signals (chemotactic cytokines): Released by damaged cells to alert the body of trouble. Act as homing signals that stimulate cells of the immune system to migrate towards the source of the chemokines. Phagocytic cells are then attracted to the wound site from the blood. Neutrophils, monocytes, macrophages.Macrophages phagocytose pathogens: Phagocytosis is a type of bulk transport into the cell in which large extracellular cargo is brought into the cell and broken down. In our example, the bacterium will eventually be broken down and the macrophage will go on to engulf and destroy other pathogens.Clinical signs of inflammation Result from innate immunity activation. Redness, heat, swelling, and pain are all classically accepted signs of inflammation. Importantly, inflammation can result in impairment in function.If the innate branch is unable to fight off the invading pathogens on its own, the adaptive branch is called in to help. Adaptive Immune BranchSpecific, slow, systemic, memoryThe adaptive branch is: Specific (it can distinguish specific species of pathogens) Slow (responses occur within days of infection). Systemic (NOT restricted to the initial site of infection). Has memory (it mounts a faster and even stronger attack against repeat pathogens).Actors of the Adaptive SystemAdaptive immunity is further divided into humoral immunity and cell-mediated immunity.Humoral immunity: B cells (matured into plasma cells) producing antibodies (Y-shaped proteins)Cell-mediated immunity: Cytotoxic T cells recognize infected cells and kill them while helper T cells act as the general of the immune army and release chemical signals that activate various immune cell typesHumoral ImmunityLymphoid tissue is the home of many types of immune cells.Plasma cells reside in the lymphoid tissues: - Plasma cells are activated and matured B cells (B cells and T cells are the two adaptive immune cell types). - Plasma cells pump out antibodies.Antibodies are Y-shaped proteins that recognize antigens from the invading pathogen.The antibodies produced by plasma cells are released into the blood vessel where they travel throughout the body.In the tissues, we show an antibody binding two viruses. Neutralizing antibodies are able to bind to viruses and toxins in such a way as they are no longer able to infect or cause damage.Cellular ImmunityThe major cells of cell-mediated immunity are the T cells, which are divided into cytotoxic T cells or helper T cells.Cytotoxic T cells have receptors on their surfaces that bind infection signals on infected host cells. The cytotoxic T cell has a receptor on its surface that is able to bind the infected cell's signal. When this happens, the T cell releases death signals which kill the infected cell.Helper T cells act as the general of the immune army. They release activation signals (cytokines and chemokines) that help phagocytic cells to perform their job more efficiently. They also release signals that activate cytotoxic T cells. B cells also receive activation signals from helper T cells.With all of these cells working together, the immune system is usually able to destroy the invading pathogens.

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ELISA Its simple ,nearly as sensitive as radioimmunoassay It has wide range of application Used for detection of specific antigen/antibod...

Virus Morphology & ClassificationOverviewViruses are obligate intracellular parasites: they rely on host cellular energy and proteins for their own replicationThe nucleocapsid comprises the viral genome, which consists of either DNA or RNA, surrounded by a capsid.The capsid is a protein coat that protects the genome.Some virions are enclosed by an envelope, which is made of lipids, proteins, and glycoproteins.Virions come in a range of sizes, from 20-400 nanometers Nucleic AcidsComprise the viral genome. Can be linear or circular.DNA Single- or double-stranded DNA.RNA Most are single-stranded. Classified according to the polarity of their RN: Positive-sense = the RNA is like messenger RNA Negative-sense = they are like templates for messenger RNA that have to be transcribed into positive RNA. Be aware that there are exceptions and complications to this classification system, which we'll learn more about in our tutorial on Virus Replication. Common capsid shapesHelical: The viral genome is enclosed by the helical capsid proteinsIcosahedral capsid: Comprises 20 equilateral triangles that that form a "shell" around the genome. The viral genome is inside the capsid. Viral attachment proteins extend from the corners of the capsid triangles.Bacteriophages: Complex capsids to facilitate invasion of bacterial cells. Comprises a viral genome enclosed within an*icosahedral head, and a tail that facilitates delivery of the viral genome into the bacterium. Viral EnvelopeThe viral envelope is linked to the viral core via matrix proteins.The envelope is acquired from the host cell during budding (a final step of viral replication).Envelope glycoproteins are on the surface. These projections facilitate entry into host cells and stimulate the immune response.Naked Capsid Virions vs. Enveloped Capsid VirionsNaked, aka, non-enveloped capsids: Relatively stable. Resistant to temperature changes, acids and proteases (including those found in the host's stomach), detergents, and drying. Thus, they can survive outside the host and are spread easily, for example, via the fecal-oral route.Enveloped capsids: More fragile. Labile to heat, acids, detergents, and drying. Thus, transmission is often via respiratory or sexual routes.

Microorganisms can be classified as obligate aerobes, facultative, microaerophilic, aerotolerant and obligate anaerobes based on their oxygen requirements.

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Kids problem solve their way through this free escape room to prevent a disease pandemic!

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One of the best methods to determine the number of bacteria present per mL of liquid broth/specimen.

Overview Two forms of acutely presenting neuropathies: • Demyelinating, typically Guillain-Barré syndrome (GBS), also called acute inflammatory demyelinating polyneuropathy – importantly, because it is inflammatory, it responds to immune-modulating therapy. • Axonal. Notably, the immune-mediated axonopathies, which are most commonly due to the primary vasculitis (eg, polyarteritis nodosa) and secondary vasculitis (eg, rheumatoid arthritis).Guillain-Barré syndrome: acute inflammatory demyelinating polyneuropathy Overview • This acute polyneuropathy characteristically presents with ascending numbness and weakness and lower motor neuron findings (eg, muscle cramps). • They occur one to two weeks following a viral respiratory or GI illness (~70% of the time). - Campylobacter jejuni, which causes diarrhea, is the most common infectious agent (up to 40% of cases in the US are due to Campylobacter jejuni). Presenting Pattern: Ascending Numbness/Weakness • Low back (and/or thigh pain) is one of the most common presenting features. • Rule out spinal cord compression or cauda equina syndrome in patients with GBS-like presentations. • The classic pattern in GBS is symmetric, ascending numbness, followed by severe weakness (often to the point of paralysis) and diminished or absent muscle stretch reflexes over a 2 – 4 week time period. - Note that because GBS is actually a polyradiculopathic neuropathy (meaning that both the nerve roots and nerves are affected), it can present with proximal (rather than distal) weakness. - As well, note that the large fiber sensory exam, itself, can be surprisingly preserved in patients despite the prominent numbness, which can be misleading. • Autonomic dysfunction (gastric hypomotility, urinary retention, cardiac dysrhythmias, and blood pressure swings) can plague patients with GBS. • There can be rapid swings in heart rate and blood pressure. - To remember these swings, it's helpful to imagine competing vagal nerve dysfunction and surges in the sympathetic nervous system. • Facial weakness and bilateral ptosis represent the oculobulbar palsies that occur in roughly half of GBS cases. - In addition to this ptosis, patients can have ocular dysmotility and pupillary changes. • Respiratory failure. - Almost one-third of patients will develop phrenic nerve failure with resultant diaphragmatic paralysis and require mechanical ventilation. - Even in the absence of diaphragmatic paralysis, patients can require intubation for airway protection from the bulbar dysfunction, itself. Treatment • Plasmapheresis or IVIG are immunotherapies. - The argument as to which is more preferred is beyond our scope here but it should be noted that to date there is not evidence for the combined use of these treatments (although this is often done in clinical practice) and it's also important to realize that steroids have been shown to be detrimental in GBS treatment. • Most importantly, management involves monitoring for respiratory failure with frequent respiratory measurements (forced vital capacity and negative inspiratory force). • And monitoring for other aspects of autonomic dysfunction, as well. These include: - Cardiovascular swings, which can occur rapidly, so we have to be careful not to overcorrect any single finding because the pendulum can rapidly swing the other way. - Cardiac dysrhythmias, which can be so severe as to require a temporary pacemaker to avoid asystole and sudden cardiac death. - Ileus, which is so common, that all patients require a good, proactive bowel protocol.Laboratory Testing in Guillain-Barré Syndrome Cerebrospinal Fluid (CSF) • CSF testing is the primary, key helpful diagnostic test; it demonstrates a mildly elevated protein (~ 60) in the setting of a normal WBC (<50), which is called cytoalbuminologic dissociation. - CSF protein is elevated because the attack affects proximal roots, which lie within the spinal canal, thus the proteinaceous debris increases the CSF protein level. Electromyography(EMG)/Nerve Conduction Studies (NCS) • EMG/NCS testing shows demyelination. - Take note, however, that the classic changes, such as prolonged distal onset latency, reduced conduction velocity, and conduction block can take several days to a couple of weeks to appear, so we look for other changes early on such as abnormal F-waves and H reflexes. Imaging • Imaging of the spine (ideally, MRI) (and brain), mostly to rule-out other potential mimickers such as cord compression and carcinomatous meningitis but also to assess for evidence of cranial nerve or nerve root enhancement. HIV • Indicate that HIV testing is warranted in GBS because HIV seroconversion, itself, can trigger an acute inflammatory demyelinating polyneuropathy (AIDP).Key Mimickers • Compressive myelopathy, which can present with an acute/subacute flaccid paraparesis (spinal shock). • Tick paralysis, which typically manifests with an abrupt (sometimes overnight) development of severe weakness (which can be asymmetric) or ataxia. - Less commonly, it can manifest with a GBS-like ascending paralysis. - Like GBS, tick paralysis will often cause sensory symptoms with negligible sensory exam findings and loss of muscle stretch reflexes. • Viral myelitis, which can initially present with a flaccid paralysis. - As well, consider that, especially in the immune-suppressed, CMV can cause an associated a radiculomyelitis that mimics GBS very closely: ascending flaccid paralysis with sensory loss. Prominent bladder and bowel incontinence is an associated finding. • Critical illness neuropathy can mimic GBS. - As its name suggests, it occurs in the setting of severe physiological stress. • Acute intermittent porphyria can cause an acute attack of cranial neuropathies and quadriparesis that resembles GBS. - It is preceded by a few days of colicky abdominal pain and behavioral disturbance. - Distinguishing features are the marked asymmetry found in porphyria; predilection for proximal muscles; and a characteristic shield-like sensory loss over the chest. - Screening involves 24-hour testing looking for abnormal levels of porphyrin in the urine or feces. - Numerous medications are implicated as the cause of a porphyria attack, they include: barbiturates, sulfonamides, and certain antiepileptics (eg, valproic acid, carbamazepine, and primidone). - Alcohol is also an important potential trigger. • Lastly, always consider B12 deficiency myelopathy, especially given its treatability.Guillain-Barré Syndrome Variants • Acute motor axonal neuropathy (AMAN) (aka Chinese paralytic illness), which has a more rapid and severe progression than AIDP, and acute motor and sensory axonal neuropathy (AMSAN): both of these axonal variants are highly associated with Campylobacter Jejuni infection. • Miller Fisher Syndrome (MFS), which consists of the triad AOA, which stands for ataxia, ophthalmoplegia, and areflexia and highlights the prominent, early oculobulbar involvement, ataxia out of proportion to weakness, and lower motor neuron findings of areflexia (rather than upper motor neuron signs found in cerebellar disorders). Anti-GQ1b IgG testing is a helpful diagnostic tool in this disorder.Review nerve conduction physiology

Classification of viruses on the basis of genome. Viral nomenclature has used a variety of virion features. Effort to classify viruses

A comic book on immunology.

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We often feel redness, heat, swelling and pain at the site of wounds. Actually this is body’s defence mechanism to destroy the pathogen. ...

Borrelia & Leptospira (Lyme Disease, Relapsing Fever)Here we will learn about infections caused by the non-Treponemal Spirochetes Borrelia and Leptospira, with a focus on Borrelia. BorreliaCauses relapsing fever and Lyme diseaseLarge, coiled Spiroche

ELISA Its simple ,nearly as sensitive as radioimmunoassay It has wide range of application Used for detection of specific antigen/antibod...

This is the print set of Resting Platelets & Activated Platelets. YOU WILL RECEIVE: 2 prints Frame is not included for this art.

The complement pathways is a part of the innate immune system and consists of a series of proteins that interact with one another.

DNA replication is an extraordinarily important and complex process upon which all life depends. During DNA replication, the two strands of

9th Edition

SUMMARY The innate immune system constitutes the first line of defense against invading microbial pathogens and relies on a large family of pattern recognition receptors (PRRs), which detect distinct evolutionarily conserved structures on pathogens, ...

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