Infectious Diseases Flashcards
How does the keratinised intact epidermis of the skin protect against infection?
Mechanical barrier, low pH, produces antimicrobial fatty acids and defensins
The GI tract has numerous defensive systems against infection. What are three ways that pathogens may establish symptomatic GI disease?
- Toxin production
- Bacterial colonisation and toxin production
- Adhesion and mucosal invasion
What are the five routes of entry of microbes?
Skin, GI tract, Respiratory tract, Urogenital tract, Vertical transmission
What are six strategies of immune evasion by microbes?
- Antigenic variation
- Inactivating antibodies or complement
- Resisting phagocytosis
- Suppressing the host adaptive immune response
- Establishing latency
- Infecting and disabling or killing immune cells
What are three mechanisms by which viruses damage or kill the host cells they have infected?
- Direct cytopathic effects (e.g. preventing synthesis of critical host macromolecules, activating pro-apoptotic pathways)
- Antiviral immune responses
- Transformation of the infected cell (oncogenic viruses)
What is quorum sensing in bacteria?
A process by which bacteria coordinately regulate gene expression within a large population through the secretion of autoinducer molecules.
What are two surface structures bacteria use to attach to host cells and tissues?
- Adhesins
- Pili (with a variable tip fibrillum)
What is bacterial endotoxin?
A lipopolysaccharide (LPS) in the outer membrane of gram-negative bacteria that both stimulates host immune responses and injures the host (generally by over stimulation). Specifically lipid A, the part of LPS that anchors it in the host cell membrane has the endotoxin activity.
What are three broad categories of exotoxins?
- Enzymes
- Toxins that alter intracellular signalling or regulatory pathways (usually enzymatic A subunit and binding B subunit that binds cell surface receptors and delivers A subunit into the cytoplasm)
- Superantigens
What are the five major histologic patterns of tissue reaction in infections?
- Suppurative inflammation
- Mononuclear and granulomatous inflammation
- Cytopathic-cytoproliferative reaction
- Tissue necrosis
- Chronic inflammation and scaring
What is suppurative inflammation characterised by and what kind of infections tend to cause this?
Increased vascular permeability and leukocytic infiltration, predominantly of neutrophils. Mostly extracellular gram-positive cocci and gram-negative rods
What is the acute development of predominantly mononuclear infiltrates often in response to?
Viruses, intracellular bacteria or intracellular parasites
What are two organisms that secrete powerful toxins which cause such rapid and severe necrosis that tissue damage is the dominant feature of infection?
Clostridium perfringens and corynebacterium diphtheriae
The diagnosis of mumps is usually made clinically (pain and swelling of salivary gland, aseptic meningitis, testis, ovary and pancreatic manifestations), what can be used for definitive diagnosis?
Serology or detection of viral RNA in salvia
The diagnosis of poliovirus can be made by viral culture, or detection of viral RNA in throat secretions or stool, or by serology.
What is the range of manifestations it can present with?
Most are asymptomatic, then from mild self-limited infections to paralysis of limb muscles and respiratory muscles. (about 1 in 100 will invade the CNS)
Viral hemorrhagic fever is a severe life-threatening multisystem syndrome in which there is vascular damage leading to widespread haemorrhage and shock. Humans are incidental hosts for most virus that cause this. What is a famous example of one that can transmit human to human?
Ebola virus
The clinical manifestations of dengue virus infection vary from fever with headache, macular rash and severe myalgias (breakbone fever) to severe dengue with bleeding, liver failure, reduced consciousness, organ failure and plasma leakage leading to shock and respiratory distress.
What is believed to cause most severe cases of dengue
Reinfection with a different strain to one of the four serotypes in a person who has already been infected before. (Thought being cross-reactive antibodies enhance uptake of virus into macrophages)
VZV is diagnosed by viral culture, PCR, or detection of viral antigens in cells scraped from superficial lesions.
Where does it establish a latent infection?
In sensory ganglia, particularly in neurons and satellite cells around neurons in the dorsal root ganglia
For the following four forms of CMV infection, describe the clinical manifestations and in the indicated list the laboratory tests that may be performed:
1. Congenital infections (and tests)
2. Perinatal infections
3. CMV mononucleosis (and tests)
4. CMV in immunosuppressed adults (and tests)
- 95% asymptomatic. Cytomegalic inclusion disease - IUGR, jaundice, hepatosplenomegaly, anaemia, thrombocytopenia, encephalitis. Fatal cases often microcephaly. Survivors often have permanent deficits. (viral culture or PCR amplification of viral DNA in urine or saliva)
- Usually asymptomatic but will shed virus for months to years. Rarely interstitial pneumonitis, FTT, rash or hepatitis
- Nearly always asymptomatic. Most common manifestation is mononucleosis-like illness (serology)
- Serious, life-threatening disseminated CMV primarily pneumonitis (can lead to acute RDS) and colitis (necrosis and ulceration can lead to pseudomembranes and debilitating diarrhoea). (Characteristic morphological alterations in tissue secretions, viral culture, rising antiviral titre, PCR based detection of CMV DNA)
What is the characteristic morphology of cells infected with CMV?
Often enlarged, cellular and nuclear pleomorphism. Prominent intranuclear basophilic inclusions usually set off from the nuclear membrane by a clear halo.
What three findings, in the order of increasing specificity, does the diagnosis of EBV depend on?
- lymphocytosis with the characteristic atypical lymphocytes in peripheral blood
- a positive heterophile antibody reaction (monospot test)
- a rising titre of specific antibodies for EBV antigens (viral capsid antigens, early antigens or EBNA)
Staphylococcus aureus (g +ve) produces a multitude of virulence factors including super-antigens. It causes pyogenic inflammation that is distinctive for it’s local destruction of host tissue. What are 6 forms S. aureus infection can take?
- Skin infections (abscess, furuncle, carbuncle, impetigo, wounds)
- Food poisoning
- Respiratory infection
- Osteomyelitis
- Endocarditis
- Toxic shock syndrome
Streptococci (g +ve) cause suppurative infections of the skin (eg erysipelas, scarlet fever), oropharynx (eg streptococcal pharyngitis), lungs and heart valves. They are also responsible of a number of post infectious syndromes such as:
Rheumatic fever, poststreptococcal glomerulonephritis and erythema nodosum
What bacteria (and of what subgroup) can cause pharyngitis, scarlet fever, erysipelas, impetigo, rheumatic fever, toxic shock syndrome, necrotising fasciitis and glomerulonephritis?
Streptococcus pyogenes (B-haemolytic group A)
Enterococci are low-virulence bacteria with an antiphagocytic capsule. They have emerged as pathogens primarily due to their resistance to antibiotics. What other class is of bacteria are they difficult to morphologically distinguish from and why?
Streptococci - as are also gram positive cocci that grow in pairs and chains
Briefly describe how immunity to M. tuberculosis (acid-fast, weakly g +ve) is primarily mediated
By Th1 cells (can take 3 weeks to start), which stimulate macrophages to kill the bacteria (even those within phagosomes where maturity was blocked by the bacterium). Accompanying tissue destruction.
