Infection and Inflammation Flashcards

1
Q

List points in the viral replication cycle where the immune system can act.

A

Some defensive strategies of the immune
system are directed against free virus particles, destroying them directly or neutralising their ability to infect cells. Other strategies are directed at the infected cells, either blocking virus replication, or killing the infected cells.

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2
Q

Outline the antiviral effects of antibodies and the antigenic variation of the influenza virus.

A
  • The antibody can block the binding ability and therefore the entry of the virus to cells by attaching to their antigens. They also activate intracellular degradation via TRIM21. TRIM21 can trigger ubiquitination of the virus to target it for degradation by proteasomes.
  • An antibody and a complement of proteins can damage enveloped viruses and carry out opsonization for phagocytosis.
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3
Q

Describe the sequence of innate and adaptive defence mechanisms employed against intracellular viruses.

A

Antibodies cannot enter the cytoplasm of the cells if not already bound to the virus upon its entry into the cell. Production of cytokines, particularly interferons, natural killer cells and the T-mediated killing of infected cells all work together synergistically to fight the infection.

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4
Q

Outline the production and activities of type I interferons.

A

Interferon-interferon receptor reaction between the surfaces of other cells introduces an antiviral state. Enzymes are activated which bring about resistance to viruses, such as degrading viral mRNA and inhibiting protein synthesis.

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5
Q

Describe the recognition of infected target cells by CD8 cytotoxic T cells.

A

Some proteins in the virus are degraded, and the polypeptide is bound to the HLA Class I protein. This complex is expressed on the surface of the infected cell and acts as a target for recognition by a cytotoxic T cell that is specific to that viral peptide. The cytotoxic T cell then kills the infected cell.

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6
Q

Describe the recognition of target cells by natural killer (NK) cells (large granular lymphocytes).

A
  • antibody-dependent cellular cytotoxicity. NK cells have Fc gamma receptors on their surface, so can be a target for recognition for antibodies specific to an antigen.
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7
Q

Explain how NK cells distinguish target cells to be killed from normal cells that should not be killed.

A

The NK mechanism of target cell recognition depends on the fact that the NK cells contain two types of receptor molecules. When the virus binds, a positive signal is sent to the NK cell to kill the virus. The use of two receptors stops normal cells being killed, as the second receptor sends a dominant inhibitory signal.

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8
Q

Describe the processes of target cell killing by NK cells and cytotoxic T cells.

A

Killer cells have granules in their cytoplasms called perforins and granzymes, which are secreted onto the surface of target cells.

Perforins perforate the membranes of the target cells. Water moves in, leading osmotic lysis. Perforins also allow granzymes to enter the cytoplasm of the target cell, activating the cell’s caspase enzymes, which activate endonuclease enzymes, which induce apoptosis of the target cells.

Killer cells can also express fas ligand on their surface, which binds to the protein as if it is expressed on the target cell, leading again to programmed apoptosis via caspase and endonuclease enzymes. Killer cells also produce type 2 interferon (IFN-), that has anti-viral activity and enhances HLA class I and class II expression.

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9
Q

Outline the functions of skin and describe how skin structure facilitates these.

A

protection - against UV light, infection, keratin

waterproof - the sensation of touch, temperature and pressure, phospholipid

thermoregulation - vasodilation/constriction, erector pili muscles, hair follicles

metabolism - synthesis of vitamin D3, fat is energy store.

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10
Q

Describe the structure and contents of the layers of the skin: epidermis, dermis and hypodermis, including the blood supply

A

epidermis - stratified squamous, forms keratinocytes

dermis - connective tissue formed of fibroblasts, collagen I, elastin, blood, nerves and receptors. It is divided into the papillary and the reticular dermis

hypodermis - formed of adipose tissue and main blood supply

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11
Q

Describe the detailed structure and cell types of the epidermis of skin and relate them to their functions, including the processes of keratinisation and pigmentation

A

Keratinocytes - formed of stratified squamous keratinising epithelial cells and produces keratin.

Melanocytes - pigment synthesising cells responsible for skin and hair colour.

Langerhans cells - communicate with the immune system.

Merkel cells - neuroendocrine function.

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12
Q

Outline some pathologies arising from defects in skin structure

A

albinism, vilitigo, basal cell/squamous cell carcinoma, melanoma, epidermolysis bullosa

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13
Q

Explain the purpose and structure of the skin appendages, glands and sensory organs

A

sensory nerve endings - responsible for deep pressure and vibration.
meissner’s corpuscle - rapidly adapting mechanoreceptors for light touch and pressure sensation.

ruffini corpuscle - mechanoreceptors, and is used in the stretching of the skin.

efferent nerve endings - control vessel diameter and blood flow and send information to sweat glands and arrector pili muscles.

Eccrine sweat glands are a dermal-subcut junction of all skin and produce sweat. The ducts open onto the skin surface and have a role in thermoregulation.

Apocrine sweat glands are localised on the axilla/groin and are used in scent production. They open into hair follicles above the sebaceous duct. They are functional at puberty.

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14
Q

Explain how skin structure varies with function in different parts of the body; recognise and explain the difference between thick and thin skin

A

Thin skin is present in most locations. This epidermis has less well defined rete ridges, a thinner keratin layer, and lots of eccrine glands. Thick skin is present on the fingertips and soles of feet. It is characterised by thick epidermis and thick keratin layer, well developed rete ridges, and lots of eccrine glands, with no hair.

Hairy skin is present on the scalp, axilla and groin. It has a thin epidermis, lots of hair follicles and sebaceous glands. In curly hair, the follicles are oblique. Lots of apocrine glands in the axilla and groin.

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15
Q

To describe how cells adapt to changes in their environment

A

maintain homeostasis, atrophy, involution, metaplasia, hypertrophy, hyperplasia

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16
Q

To establish the possible outcomes of inflammation

A

resolution, repair (fibrosis/scarring), chronic inflammation, or abscess formation

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17
Q

To define the capacity of different tissues to regenerate and repair

A

Labile cells can resolve damage.

Stable cells are capable of regeneration and so can resolve or scar.

Permanent, non-dividing cells will always scar and have a consequent loss of function.

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18
Q

To describe the process of tissue resolution and repair and the differences between them

A

Resolution arises from damage to parenchyma in labile or stable tissues. The damaging stimulus is removed, and inflammatory cells, mediators and exudate are introduced. Injured cells are replaced by regeneration, and this restores normal function. There is minimal or absent evidence of damage.

Repair arises from damage to parenchyma and stroma (or in the brain or muscle). The damaged tissue is replaced with connective tissue. Formation of granulation tissue and scar tissue occurs. The tissue is remodelled for strength and lacks the functional capabilities of the damaged tissue.

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19
Q

To describe the process of wound healing in relation to skin

A

inflammatory phase - acute inflammation and the arrival of macrophages which produce growth factors for the next phase occurs.

proliferative phase - granulation tissue is formed, building tissue to fill the wound. Fibroblasts secrete matrix components, growth factors to stimulate angiogenesis, and epithelial cells to regrow over the wound.

remodelling phase - remodelling/organisation of the matrix takes place to develop appropriate tissue architecture for the function of the tissue. Due to the action of fibroblasts laying down collagen and collagenases breaking down collagen to orientate for maximal tensile strength. Wound contraction and decreased vascularity follows.

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20
Q

To list mediators of the repair process

A

growth factors, which are hormone-like molecules that stimulate proliferation, differentiation and the maturation of cells. In healing they attract endothelial cells and fibroblasts and therefore have a role in angiogenesis and the production of the extracellular matrix.

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21
Q

To consider examples of scarring causing disease (fibrosis)

A

Pathological fibrosis occurs where repair is the problem. In the liver, this is cirrhosis. In the lung, this is interstitial fibrosis, such as asbestosis.

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22
Q

Outline different social-cognition models of health behaviour change including the Health Belief Model and the Theory of Planned Behaviour.

A

Health Belief Model - useful to help to predict, understand and address non-adherence to treatment. It is better at predicting initiation of health protective behaviours (such as screening) than reducing health risk behaviour (such as smoking)

Theory of Planned Behaviour - idea of perceived behavioural control. It suggests what constraints might be on a person to stop them from doing a particular behaviour, intentions don’t always turn into actions.

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23
Q

Understand the role of patient motivation and self-efficacy in behaviour change.

A

people are influenced by factors in their life when it comes to undertaking health behaviours

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24
Q

Apply psychological theory to the design of individualised interventions to improve patients’ health-related behaviour.

A

The health belief model ensures people understand threat, minimise barriers, increase cues to action and increase self-efficacy. The planned behaviour model thinks about people’s resources and opportunities, and what normative beliefs they might have.

We must understand how a person’s societal norms might influence their ability to complete the behaviour. Social cognition also plays a role.

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25
Q

Apply Motivational Interviewing approaches to health-related behaviour change.

A

Motivational interviewing is a type of counselling that is patient centred that acts to explore and resolve ambivalence about behaviour change. It is useful for people who are unmotivated and unprepared for change. It is not as useful for people who are already motivated to change. The idea is to increase motivation, and then make a commitment to change.

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26
Q

Defining health beliefs and culture

A

Culture is an umbrella term which encompasses the social behaviour and norms found in human societies, as well as the knowledge, beliefs, arts, laws, customs, capabilities and habits of the individuals in these groups.

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27
Q

Concept of cultural competency

A

Cultural competence is the ability to understand, communicate with and effectively interact with people across cultures. Cultural competence encompasses. being aware of one’s own world view. developing positive attitudes towards cultural differences.

28
Q

Awareness of some key features of major religions / faiths & how they can affect the provision of health care, eg death & dying

A
muslim - burial asap
jew - burial asap
hindu - cremation within 12 hours
buddhist - cremation in 3 to 7 days
sikh - cremation asap
christian - burial (cremation), no time specicifity
29
Q

To be aware of the role of a person’s spiritual life and their identity

A

culture can change throughout generations:

arrival - culture of origin
2nd generation - adopting some indigenous practices
3rd generation - mostly indistinct from culture of origin but may have recognisable differences (e.g. food/religious belief)

30
Q

Describe the basic legal process in the UK

A

The ‘common law’ means the substantive law and procedural rules that have been created by the judges through the decisions in the cases they have heard.

Statute law, on the other hand, refers to law that has been created by Parliament in the form of legislation.

31
Q

Identify components of the Human Rights Act

A
  • Article 2 Right to life
  • Article 3 Freedom from torture and inhuman or degrading treatment
  • Article 4 Freedom from slavery and forced labour
  • Article 5 Right to liberty and security
  • Article 6 Right to a fair trial
  • Article 7 No punishment without law
  • Article 8 Respect for your private and family life, home and correspondence
  • Article 9 Freedom of thought, belief and religion
  • Article 10 Freedom of expression
  • Article 11 Freedom of assembly and association
  • Article 12 Right to marry and start a family
  • Article 14 Protection from discrimination in respect of these rights and freedoms
32
Q

List differences in biological and physical properties between viruses and bacteria.

A

viruses are much smaller than bacteria and are not living - they are nucleic acids surrounded by a protein capsule. they undergo independent synthesis of their components

33
Q

List the essential components of viruses, and their functions.

A

nucleic acid - genome of virus

protein coat - capsid for protection, mediate attachment to cells, enzymes for macromolecular synthesis, avoid immune recognition, antiapoptotic

lipid - makes virus more fragile

34
Q

Outline the basis of viral classification into families, genera, and strains.

A

First, the nature of the genetic material should be understood, then the nature of the capsid and if the virus is enveloped or not. Seeing the size and shape of the virus can be useful, but is not always possible. Viruses can be split into families, genera and strains.

35
Q

Describe the main steps involved in viral replication.

A
  1. attachment of viral ligand to receptor
  2. entry of virus by endocytosis
  3. dissolution of protein capsule
  4. macromolecular synthesis
  5. assembly
  6. released by budding or cell lysis
36
Q

Define the terms virion; genome; capsid; envelope; the Baltimore classification of viral replication; reverse transcriptase; retrovirus.

A

viron - mature form of virus
capsid - protien capsule protecting virus
retrovirus - a type of virus that has RNA instead of DNA as its genetic material. It uses an enzyme called reverse transcriptase to become part of the host cells’ DNA.

37
Q

Identify and understand your role as a doctor and a communicator

A

The role of a doctor is to return their patient to health and social obligations, to provide a quality of care, to listen and empathise, to use expert knowledge and skills, to maintain confidentiality, to provide leadership and work as a team. A doctor is in a powerful position to influence the patient.

38
Q

Describe how the doctor and patient role has changed over time

A

Historically, the ruling class had power and doctors would work in exchange for a small fee. The patient’s body, spirituality and emotional wellbeing was important. As time went on, there was a growing distance between the patient and the doctor. Symptoms became secondary indicators of disease and diagnosis was based on the examination of external structures.

In laboratory medicine, scientific medicine emphasised the use of objective lab tests to identify morbid processes. The current approach is patient-centred care. There is equality, and a patient’s concerns are acknowledged and considered. The doctor establishes the patient’s agenda, listens and reflects, uses open questions, and observes, encourages, clarifies, and seeks patients’ ideas, empowering them. The patient is an active participant, asks questions and influences the course of the consultation.

39
Q

Describe how power dynamics can affect communication between doctor and patient, and can influence patient behaviour

A

The goal is an adult-adult relationship, not an adult-child relationship. We should ensure concordance between patients and doctors. A lack of concordance leads to paternalism. Empowerment isn’t always possible but it is the goal.

40
Q

Apply this information to conduct a patient-centered consultation

A

A good relationship should be egalitarian, and not a power imbalance. Patients can express all reasons for coming (their symptoms, thoughts, feelings, and expectations). The patient leads in areas where he/she is the expert, such as their symptoms, preferences, and concerns.

The doctor leads in areas where he/she is expert, such as the details of disease, and treatment. The doctor’s role is a facilitator of patient participation, interpreter and a synthesiser of information.

41
Q

List the routes by which viruses spread from one individual to another.

A

Viruses can shed in skin via vesicles, through the respiratory tract via droplet, through the gastrointestinal tract via saliva and faeces, through the urogenital tract via urine, semen, and female genital tract secretions, through the blood and through breast milk.

42
Q

List four possible outcomes of virus infection of a cell and give examples of each.

A

cell death

chronic infection

latency

transformation

43
Q

Changing NHS culture

A

change is often driven by society or politicians

44
Q

Identify three cytokines involved in longer term (> 24 hours) inflammation and describe three principal biochemical changes that lead to degradation of damaged tissue and preparation for healing.

A
  • interleukin-1 and tumour necrosis factor
  • Leukocyte production of proteolytic enzymes and oxygen radicals
    leads to breakdown of tissue in preparation for repair.
45
Q

Describe the functions of neutrophils, monocytes and platelets attracted to sites of injury during the delayed phase of an inflammatory response and the subsequent proliferative and granulation phase.

A
  • Macrophages and platelets produce growth factors
46
Q

Describe the function of the maturation phase wound healing and identify one major factor that will interfere with this process.

A

This phase is associated with a cessation of the proliferation phases and the remodelling of the tissue. There is evidence for the involvement of macrophages. However, wound closure is not the end point for the healing process.

At the site of injury, there is reduced vascularisation that lessens the demand for nutrients as metabolic activity of the tissue declines. There is remodelling of collagen and the reinnervation of nerves. The increases the strength of tissues and the return of sensation, but there is a lack of elastic in scar tissue.

47
Q

Explain the anti-inflammatory action of cyclooxygenase inhibitors by reference to changes in the microcirculation.

With the aid of a diagram describe the principal effects of glucocorticoid steroids on humoral and cellular factors implicated in long-term inflammatory responses.

A

NSAIDS are competitive inhibitors of cyclooxygenase and reduce inflammation by suppressing PG synthesis. They lead to reduced vasodilatation and hyperaemia, reduced hydrostatic pressure in venules, reduced protein leakage into extracellular space, and reduced pain.

There is a topical formulation of NSAIDs to reduce gastrointestinal side effects.

for glucocortiods, long term treatment inhibits inflammation at several steps in the process by reducing prostanoid and leukotriene production and, therefore, inflammatory synergy between humoral and cellular factors. There is action at the level of phospholipase A2 (induction of lipocortin), COX-2 and iNOS.

There is expression of cell adhesion molecules, chemotaxis of neutrophils, and cytokine production. It potentiates vasoconstrictors. The short term effects differ.

48
Q

Outline the clinical and pathological features of clinical cases involving common instances of pathological cell degeneration and death (fatty change of liver, paracetamol poisoning, acute tubular necrosis of kidney, Alzheimer’s disease).

A

liver - Long term consequence is hepatic cirrhosis following ethanol poisoning, malaise, nausea and vomiting

paracetamol poisoning - drowsy, liver toxin, liver function test carried out, Liver cells eosinophilic
Nuclei show pyknosis and karyorrhexis, Hepatic necrosis due to paracetamol
Necrosis takes place in the centriacinar hepatocytes
These are rich in esterases which produce a toxic intermediary from paracetamol
Periportal hepatocytes lack high levels of esterases and survive

acute tubular necrosis of kidney - Pale and shocked, semi-conscious, Problems in maintaining blood pressure continued, Cause of damage is poor blood flow and possibly hypoxia to the kidney
Tubule is most sensitive part of the kidney to this type of damage
Renal function recovers when the tubular epithelial cells regenerate

alzheimer’s - Impaired recent memory, impaired ability to name objects, impaired ability to draw simple shapes, Temporal lobe atrophy, Parietal lobe atrophy, Severe atrophy of temporal lobes with lesser degree of atrophy of parietal and frontal lobes

49
Q

Define the following terms cytolytic infection; cytopathic effect; chronic or persistent infection; viral latency; transformation.

A

cytolytic infection - kill host cell
cytopathic effect - structural changes in a host cell resulting from viral infection
latency - where there is no virus replication, and no production of viral proteins. Once a cell is infected, it is always infected. Virus replication can be reactivated if triggered.
transformation- which leads to the immortalisation of a cell. The cell can divide forever as long as the nutrients are available.

50
Q

List four possible outcomes of virus infection of a cell and give examples of each.

A

cell death - Rhinovirus-infected lung fibroblasts
chronic infection - hepatitis B
latency - Gingivostomatitis or orolabial herpes
transformation - Epstein-Barr virus

51
Q

List the sequence of events involved in the establishment of infection colonisation, invasion, avoidance of host defenses, tissue damage.

A

colonisation - establishment of stable population of bacteria in a host.

invasion - Once established in the body, some bacteria are able to penetrate into, through or between cells. Adhesion to specific receptors is usually the first stage in invasion via adhesins and invasins.

avoidance of host defences - bacteria can avoid complement, antibodies and phagocytes

tissue damage - caused by indirect effects of bacterial toxins, and the induction of autoimmune responses

52
Q

List common sites of entry.

A

mucosal surfaces, skin

53
Q

Outline the key bacterial factors involved in production of tissue damage.

A

There are two types of bacterial toxins. The first are exotoxins. Their actions are selective for specific biochemical targets. The second are endotoxins (LPS). These activate many biochemical pathways, and their effects are mediated by the triggering of cytokine release from mammalian cells.

54
Q

Outline the concept of virulence factors.

A

Both groups of bacteria possess virulence determinants which contribute to their ability to cause disease. The possession of a single virulence determinant is rarely sufficient to make a bacterium pathogenic. Virulence is multifactorial.

55
Q

Define the term primary pathogen and contrast with opportunistic pathogen.

A

opportunistic pathogens, which only cause serious disease when the host defence systems are impaired, and primary pathogens, which are capable of causing disease in the absence of immune defects.

56
Q

Gain an understanding of the types of bacterial pathogen

A

symbionts

commensals

opportunistic pathogens

primary pathogens

accidental pathogens

57
Q

Gain an appreciation of the multifactorial nature of infection

A

Bacteria elaborate virulence determinants. Most bacterial pathogens are multifactorial. Virulence arises from the production of an array of virulence factors, such as exotoxins and endotoxins, adhesins and invasins.

58
Q

Gain knowledge about the strategies of some pathogens to survive within their host

A

Bacteria can have immune evasion molecules, which can be complement-binding proteins, immunoglobulin-binding proteins, or protein capsules. They also have nutrient scavenging systems with siderophore/siderophore-binding proteins, and iron-binding protein receptors (transferrin, lactoferrin, and haemoglobin).

59
Q

List and describe the various patterns of tissue necrosis and their causes.

A
  • liquefactive necrosis: tissue is effaced quickly, leaving liquid and macrophages due to the release of hydrolytic enzymes.
  • coagulous necrosis: cell and tissue outlines are preserved in the initial stages. The most important cause of this is ischaemia
  • caseous necrosis: tissue appears as sheets of homogenous, unstructured proteinaceous material.
  • gummatous necrosis: has a rubbery firm texture with dense packed proteinaceous material.
  • hemorrhagic necrosis: the tissue is suffused with blood and there is red cell extravasation. It is caused by complete venous obstruction.
  • fibrinoid necrosis: occurs frequently in blood vessels. The blood vessel walls are replaced by a fibrin-like material. It is caused by severe hypertension, vasculitis or radiation damage.
60
Q

Outline the major changes which occur at the molecular level when a cell dies.

A

Cytochrome-C and other factors leak from impaired mitochondria and cause apoptosis. If there is catastrophic failure of ATP production by gross mitochondrial damage then necrosis superervenes.

61
Q

Outline the spectrum of helminths responsible for human disease.

A

Helminths can be classified into three families: trematodes, cestodes and nematodes.

Trematodes are flatworms, although some are rounded in appearance. They have two suckers for attachment to the host. The oral sucker leads to a blind ending gut. They are digenetic, meaning that they have two hosts in their lifecycle. They have a secretory system opening into an excretory pore. The rest of their body is mainly for reproduction, they are self-fertilising hermaphrodites.

Cestoda are known as tapeworms. Their body is arranged in identical individuals known as pork tapeworm attached to the intestine of an infected host using its scolex. They live in the digestive tract. This can be controlled by inspection of pork meat and the sanitary disposal of human faeces.

Nematodes are also known as roundworms. They are very diverse with around 28,000 species. They have a digestive system with a tube that opens at both ends. An example is a pinworm.

62
Q

Outline the role of vectors in the life cycle of selected helminths.

Distinguish helminthic infections that are restricted to the gut from those which invade the tissues.

A
  • Trematodes: Schistosomiasis (also known as bilharzia or snail fever) has low mortality but high morbidity. It occurs largely in developing tropical countries, in rural areas. Dams and irrigation systems have encouraged its spread. Chronic infection is a cause for significant morbidity.
  • Cestode: Hydatid disease is caused by echinococcosis. This is the dog tapeworm and lives in the dog’s small intestine. Humans are an intermediate dead-end host. Infection is acquired by ingestion of cysts from dog excreta. On infecting a human, hydatid cysts containing large amounts of the immature tapeworm.
  • Nematode: Ascaris lumbricoides is commonly known as roundworm infection. Eggs hatch, burrow through the intestine, enter the lungs and then the respiratory tract. They are swallowed and then develop into adults in the intestine. They can go unnoticed, but usually cause abdominal pain, asthma attacks and in severe cases, adult worms can invade bile ducts, the liver and the pancreas. This can be fatal. It can be treated with anti-parasitic drugs.
63
Q

Outline the different approaches to the laboratory diagnosis of helminthic infections.

Explain the principles for the prevention of helminthic infections through vector control, hygiene and sanitation, and chemotherapy.

A

Schistosomiasis can be diagnosed by looking at the ova under a microscope. For S.mansoni, ova (lateral spine) are present in faeces or rectal snips, for S. haematobium, ova (terminal spine) are present in filtered midday urine. ELISA detects antigens and antibodies and supports the parasitological diagnosis. Treatment is praziquantel (Biltricide), which is an antihelminthic effective against flatworms.

The formation of hydatid cysts occurs primarily in the liver and lungs. They grow slowly over 5 to 20 years. The pressure of the growing cyst is often the first sign of infection. The rupture of cysts can cause anaphylactic shock and can lead to dissemination due to protocolices release. Treatment is to remove the cyst through surgery, or to open the cyst and treat it.

Ascaris lumbricoides is commonly known as roundworm infection. Eggs hatch, burrow through the intestine, enter the lungs and then the respiratory tract. They are swallowed and then develop into adults in the intestine. They can go unnoticed, but usually cause abdominal pain, asthma attacks and in severe cases, adult worms can invade bile ducts, the liver and the pancreas. This can be fatal. It can be treated with anti-parasitic drugs.

64
Q

Outline the range of protozoa responsible for human disease.

List the protozoa responsible for systemic and potentially life threatening infection.

A

malaria, giardiasis, amoebiasis, leishmaniasis

65
Q

Describe the role of reservoirs (sources) and vectors in the life cycle of selected protozoa.

A

The mosquito’s proboscis penetrates the skin. Only the female drinks blood, and bites tend to happen at night. The mosquito injects sporozoites into the bloodstream. These travel to the liver and invade liver cells. Secondly, the sporozoites grow and divide into merozoites. There are tens of thousands in each liver cell.

Merozoites enter the bloodstream and invade red blood cells. Asexual reproduction releases newly formed merozoites every 1-3 days. Some merozoites stop this cycle and turn into a sexual form in the red blood cells, known as gametocytes.

The mosquito ingests red blood cells containing gametocyteswhich get released in the gut and develop into mature sex cells called gametes. Male and female gametes fuse to form a zygote which develop into ookinetes which burrow into the gut wall forming oocysts. Growth and division of oocysts produces thousands of sporozoites into the body cavity of the mosquito. These travel to the salivary glands.

66
Q

Outline the approach to diagnosis of protozoal infections.

A

Malaria is diagnosed through a blood smear. There is a thick and thin smear. Thick films allow microbiologists to screen a larger amount of blood. It is 11 times more sensitive than thin films. Thick films distort the parasite more making species diagnosis more difficult. It is usual to use both methods.

amoebiasis can be diagnosed by a fresh stool or colon biopsy, or a serum amoebic antibody test.