infection and immunity revision part 2 Flashcards
what are the 2 types of adaptive immune responses
- B lymphocytes produce antibodies which leads to HUMORAL immunity. This is associated with extracellular microbes. NOTE Th2 stimulates the humoral response
- T lymphocytes are designed to fight intracellular microbes e.g. viruses cancer cells. provides CELLULAR immunity. Th1 stimulates the cellular response
The main difference between TH1 and TH2 helper cells is that the TH1 helper cells generate immune responses against intracellular parasites, including bacteria and viruses, whereas the TH2 helper cells generate immune responses against extracellular parasites including, helminths.
can both B cells and T cells recognise antigens directly?
B cells recognise antigens directly but T cells do recognise antigens directly and can only recognise antigens that have been processed my APCs.
where are MHC I and MHC II found and what do they present to?
MHC I are present on all nucleated cells and displays its antigens to CD8+ cytotoxic T cells.
MHC II are found only on antigen presenting cells and display its antigens to CD4+ cytotoxic t cells
what is Th1 and Th2
Th1 are helper t cells that activate macrophages and Th2 activate B cells.
Th1 is involved in cellular immunity and Th2 is involved in humoral immunity.
CD4+ T cell effectors help macrophages (activated by Th1) and B cells (activated by Th2) to eliminate extracellular bacteria
• Define the terms: Normal flora; Opportunistic pathogen; pathogen; pathogenesis; virulence; colonisation and normal flora; asymptomatic carriage; infection.
Normal flora- microorganisms that live on another living organism (human or animal) or inanimate object without causing disease.
Opportunistic pathogen- An infectious microorganism that is normally a commensal or does not harm its host but can cause disease when the host’s resistance is low.
Parthenogenesis: the manner of development of a disease.
Virulence: the severity or harmfulness of a disease or poison.
Colonisation: Colonisation is when microorganisms, including those that are pathogenic, are present at a body site (E.g. on the skin, mouth, intestines or airway) but are doing no harm and are not causing symptoms of infection.
Asymptomatic carriage: person or other organism that has become infected with a pathogen, but that displays no signs or symptoms.
Colonisation describes when bacteria grow on body sites exposed to the environment, without causing any infection. This is a normal process. These bacteria may form part of the normal flora of the individual; although colonisation is not necessarily normal flora.
• List examples of bacterial virulence determinants: - e.g. adhesins, capsules, exotoxins
Factors that are produced by a microorganism and evoke disease are called virulence factors. These factors are either secretory, membrane associated or cytosolic in nature. The membrane associated virulence factors aid the bacterium in adhesion and evasion of the host cell. Examples are toxins, surface coats that inhibit phagocytosis, and surface receptors that bind to host cells.
• Describe the main stages of a bacterial infection from adherence, immune evasion, transmission to clearance
Many pathogenic bacteria colonize mucosal sites by using pili (fimbriae) to adhere to cells. They employ tactics such as modulating their cell surfaces, releasing proteins to inhibit or degrade host immune factors, or even mimicking host molecules.
• Describe the direct and indirect effects of bacterial infection that cause tissue damage
Sometimes bacteria multiply so rapidly they crowd out host tissues and disrupt normal function. Sometimes they kill cells and tissues outright. Sometimes they make toxins that can paralyze, destroy cells’ metabolic machinery, or precipitate a massive immune reaction that is itself toxic.
• List the 3 main types of bacterial exotoxins. Explain their mechanism of action and how this results in disease
There are three main types of exotoxins:
• superantigens (Type I toxins);
• exotoxins that damage host cell membranes (Type II toxins); and.
• A-B toxins and other toxin that interfere with host cell function (Type III toxins).
Superantigens are bacterial proteins that generate a powerful immune response by binding to Major Histocompatibility Complex class II molecules on antigen-presenting cells and T cell receptors on T cells.1
Superantigens have been implicated in acute human diseases such as food poisoning and toxic shock syndrome. These acute diseases can be considered to be the ‘bad” effects of superantigens.
Examples of superantigens include toxic shock syndrome toxin-1 (TSST-1), Streptococcal pyrogenic exotoxins (SPE), Staphylococcal enterotoxins (SE), and enterotoxogenic E. coli (ETEC) enterotoxin.
• Define Koch’s postulates
Koch’s postulates are a set of observations and experimental requirements proposed by Heinrich Hermann Robert Koch, intended to prove that a particular organism causes a particular infectious disease.
1- The suspected causative agent must be absent from all healthy organisms but present in all diseased organisms.
2-The causative agent must be isolated from the diseased organism and grown in pure culture.
3- The cultured agent must cause the same disease when inoculated into a healthy, susceptible orgnanism.
4-The same causative agent must then be reisolated from the inoculated diseased organism.
• Identify the role of bacterial enzymes, bacterial exotoxins and endotoxins and other causes of sepsis in disease pathogenesis
Bacteria are the most common cause of sepsis, with 62.2% of patients with positive blood cultures harboring Gram-negative bacteria and 46.8% infected with Gram-positive bacteria.
In sepsis, infection from the tissues enters to venous blood. Erythrocytes in the venous blood are lack of oxygen and sepsis-causing bacteria easily survive oxycytosis (Oxycytosis is the main mechanism of bacteria clearing from the bloodstream. In oxycytosis erythrocytes “catch” bacteria by electric charge attraction forces and kill them by oxygen released from oxyhemoglobin by producing antioxidant enzymes.) Pathogens penetrate erythrocyte membrane by hemolysins and form a bacterial reservoir inside erythrocytes.
Endotoxins are part of the outer membrane of the cell wall of Gram-negative bacteria.
• Describe the mechanism of disease in Toxic Shock Syndrome
Toxic shock syndrome (TSS) is caused from intoxication by one of several related Staphylococcus aureus exotoxins. The most commonly implicated toxins include TSS toxin type-1 ,remember superatigrn, (TSST-1) and Staphylococcal enterotoxin B. Almost all cases of menstrual TSS and half of all the non-menstrual cases are caused by TSST-1.
• Outline immunopathology as a consequence of infection including immune complex related disease, molecular mimicry, autoimmunity and infection, hypersensitivity of microbial origin
immune complex related disease- immune-complex disease describes a state in which circulating antigen–antibody complexes, formed by coexisting immune reactants, induce vascular injury.
Molecular mimicry is defined as structural similarity between antigens coded by different genes. Molecular mimicry is one of the leading mechanisms by which infectious or chemical agents may induce autoimmunity. It occurs when similarities between foreign and self-peptides favor an activation of autoreactive T or B cells by a foreign-derived antigen in a susceptible individual.
Hypersensitivity- reactions are exaggerated or inappropriate immune responses to benign antigens. It is the immune response, not the antigens that are harmful to the host.
• Describe the structure of; Human Immunodeficiency virus, herpes viruses, hepatitis A, B and C viruses, influenza virus, rota virus, norovirus, measles, mumps and rubella viruses, enteroviruses, rhinovirus and adenovirus, which diseases do each of these viruses cause
HIV- causes aids, defieciency of helper t cells symptoms of HIV: fever, chills, rash, night sweats, muscle aches, sore thoat,swollen lymph nodes
Herpes virus causes herpes
Hep a- People usually get hepatitis A from eating or drinking something that has been contaminated with a small amount of the virus, sometimes contained in fecal matter. This can happen when a person with hepatitis A infection goes to the bathroom, doesn’t wash his hands and then handles or serves food.
Hep b- sexual transmission or IV drug use.
Hep c- transmitted through direct blood contact (almost always chronic)
he symptoms of types A, B, and C may include fatigue, nausea, poor appetite, belly pain, a mild fever, or yellow skin or eyes (jaundice) due to liver damage. When hepatitis B and C become chronic, they may cause no symptoms for years.
Hepatitis A and B can be prevented by vaccination, but not hepatitis C.
All 3 are viruses
Rota virus- causes inflammation in the stomach and intestines. It can cause severe diarrhea, vomiting, fever, belly pain, and dehydration in infants, young children, and some adults.
Rhinovirus- sore throat, common cold .. also ear and sinus infections
Adenovirus- can cause cold-like symptoms, fever, sore throat, bronchitis, pneumonia, diarrhea, and pink eye (conjunctivitis). You can get an adenovirus infection at any age.
• Using Varicella Zoster virus as an example describe mechanisms that viruses use to spread within the body
How is chickenpox spread? Chickenpox is transmitted from person to person by directly touching the blisters, saliva or mucus of an infected person. The virus can also be transmitted through the air by coughing and sneezing
They work by infecting T cells and then these infected T cells can transport VZV to skin within a short time after entering the circulation.
• Grave’s disease,
this is an autoimmune thyroid disease, in healthy individual’s pituitary makes thyroid-stimulating hormone TSH which triggers them to produce thyroid hormones. Thyroid hormones engage in an inhibitory feedback loop- they stop more TSH being produced.
Graves, is an autoimmune disease characterized by hyperthyroidism due to circulating autoantibodies. Thyroid-stimulating immunoglobulins (TSIs) bind to and activate thyrotropin receptors, causing the thyroid gland to grow and the thyroid follicles to increase synthesis of thyroid hormone.
