opportunistic infections Flashcards
congential condtions primary?
Severe combined immune deficiency (SCID)
Granulocyte disorders
Chronic granulomatous disease
Bacterial infections, abscesses, invasive fungal
Staphylococcus aureus, Pseudomonas aeruginosa, Aspergilllus
T-cell
Di George syndrome
Viral infection- Herpes viruses
Intracellular bacteria- Mycobacteria (TB and atypical)
Fungal infection- Chronic candida, Cryptococcocus neoformans
Protozoal infection- Toxoplasma gondii
B-cell
Brutons disease
Chronic RTI (sinusitis pneumonia, otitis media), gastrointestinal infections
Strep pneumoniae, Haemophilus influenzae
Complement deficencies
Meningococcal disease
Others eg cystic fibrosis
digeorgs syndrome?
22q11.2 deletion syndrome, which has several presentations including DiGeorge syndrome (DGS), DiGeorge anomaly,[2][3] velo-cardio-facial syndrome, Shprintzen syndrome, conotruncal anomaly face syndrome, Strong syndrome, congenital thymic aplasia, and thymic hypoplasia, is a syndrome caused by the deletion of a small piece of chromosome 22. The deletion occurs near the middle of the chromosome at a location designated q11.2—signifying its location on the long arm of one of the pair of chromosomes 22, on region 1, band 1, sub-band 2. It has a prevalence estimated at 1:4000.[4] The syndrome was described in 1968 by the pediatric endocrinologist Angelo DiGeorge.[5][6] 22q11 deletion is also associated with truncus arteriosus (see TOF).[7]
The features of this syndrome vary widely, even among members of the same family, and affect many parts of the body. Characteristic signs and symptoms may include birth defects such as congenital heart disease, defects in the palate, most commonly related to neuromuscular problems with closure (velo-pharyngeal insufficiency), learning disabilities, mild differences in facial features, and recurrent infections. Infections are common in children due to problems with the immune system’s T-cell mediated response that in some patients is due to an absent or hypoplastic thymus. 22q11.2 deletion syndrome may be first spotted when an affected newborn has heart defects or convulsions from hypocalcemia due to malfunctioning parathyroid glands and low levels of parathyroid hormone (parathormone). Affected individuals may also have any other kind of birth defect including kidney abnormalities and significant feeding difficulties as babies. Disorders such as hypothyroidism and hypoparathyroidism or thrombocytopenia (low platelet levels), and psychiatric illnesses are common late-occurring features.[8] Microdeletions in chromosomal region 22q11.2 are associated with a 20 to 30-fold increased risk of schizophrenia.[9]
Studies provide various rates of 22q11.2 deletion syndrome in schizophrenia, ranging from 0.5 to 2% and averaging about 1%, compared with the overall estimated 0.025% risk of the 22q11.2 deletion syndrome in the general population.[10]
Salient features can be summarized using the mnemonic CATCH-22 to describe DiGeorge’s syndrome, with the 22 to remind one the chromosomal abnormality is found on the 22 chromosome, as below:[11]
Cardiac Abnormality (especially tetralogy of Fallot)
Abnormal facies
Thymic aplasia
Cleft palate
Hypocalcemia/Hypoparathyroidism.
brutons?
X-linked agammaglobulinaemia (also called X-linked hypogammaglobulinaemia, XLA, Bruton type agammaglobulinaemia, Bruton syndrome, or Sex-linked agammaglobulinaemia[1]:83) is a rare X-linked genetic disorder discovered in 1952 that affects the body’s ability to fight infection. XLA is an X-linked disorder, and therefore is much more common in males. XLA patients do not generate mature B cells,[2] which manifests as a complete lack of antibodies in their bloodstream. B cells are part of the immune system and normally manufacture antibodies (called immunoglobulins), which defend the body from infections by sustaining an immunological humoral antibody response. Patients with untreated XLA are prone to develop serious and even fatal infections. A mutation occurs at the Bruton’s tyrosine kinase (Btk) gene that leads to a severe block in B cell development (at the pre-B to immature B cell stage) and a reduced Immunoglobulin (antibody) production in the serum. Btk is particularly responsible for mediating B cell development and maturation through a signaling effect on the B cell receptor BCR. Patients typically present in early childhood with recurrent infections, in particular with extracellular, encapsulated bacteria.[3] It occurs in a frequency of about 1 in 100,000[4] male newborns, and has no ethnic predisposition. XLA is treated by infusion of human antibody. Treatment with pooled gamma globulin cannot restore a functional population of B cells, but it is sufficient to reduce the severity and number of infections due to the passive immunity granted by the exogenous antibodies.[3]
XLA is caused by a mutation on the X chromosome of a single gene identified in 1993 which produces an enzyme known as Bruton’s tyrosine kinase, or Btk.[3] XLA was first characterized by Dr. Ogden Bruton in a ground-breaking research paper published in 1952 describing a boy unable to develop immunities to common childhood diseases and infections.[5] It is the first known immune deficiency, and is classified with other inherited (genetic) defects of the immune system, known as primary immunodeficiency disorders.
congenital phagocytes?
Phagocytic
Bacterial infections
Pyogenic, abscesses
Staphylococcus aureus, Pseudomonas aeruginosa
Invasive fungal infection
Aspergillus, Candida spp
congential humoral?
Humoral immunity
Bacterial
Chronic RTI (sinusitis pneumonia, otitis media)
Strep pneumoniae, Haemophilus influenzae
GIT infection
Giardia, cryptosporidium
congenital cell mediated?
Cell mediated
Viral infection
Herpes viruses
Intracellular bacteria
Mycobacteria (TB and atypical)
Fungal infection
Chronic candida, Cryptococcocus neoformans
Protozoal infection
Toxoplasma gondii,
acquired infection?
Infection – HIV, malaria
Malignancy (especially leukaemia)
Cytotoxics
Radiation
Drugs – Corticosteroids, BRMs
Stem cell and organ transplantation
Burns and critical illness
Malnutrition
hyposplenism
staphylococcal pneumonia?
Abscess formation
disseminated disease
slow resolution
rifampicin often required
MRSA increasingly implicated
Toxin mediated disease eg PVL producing strains
disseminated?
Disseminated disease refers to a diffuse disease-process, generally either infectious or neoplastic. The term may sometimes also characterize connective tissue disease.
A disseminated infection, for example, has extended beyond its origin or nidus and involved the bloodstream to “seed” other areas of the body. Similarly, one can view metastatic cancer as a disseminated infection in that it has extended into the bloodstream or into the lymphatic system and thus “seeded” distant sites (a process known as metastasis).
Disseminated disease often contrasts localized disease.
PVL?
Panton-Valentine leukocidin (PVL) is a cytotoxin—one of the β-pore-forming toxins. The presence of PVL is associated with increased virulence of certain strains (isolates) of Staphylococcus aureus. It is present in the majority [1] of community-associated Methicillin-resistant Staphylococcus aureus (CA-MRSA) isolates studied[2][3] and is the cause of necrotic lesions involving the skin or mucosa, including necrotic hemorrhagic pneumonia. PVL creates pores in the membranes of infected cells. PVL is produced from the genetic material of a bacteriophage that infects Staphylococcus aureus, making it more virulent.[4]
listeria?
Tolerant of cold temperatures
Causes sepsis and meningo encephalitis in immunocompromised
Fetal death and neonatal infections
Sensitive to ampicillin
Ecthyma gangrenosum?
Ecthyma gangrenosum is an infection of the skin typically caused by Pseudomonas aeruginosa. It presents as a round or oval lesion, 1 cm to 15 cm in diameter, with a halo of erythema. A necrotic center is usually present with a surrounding erythematous edge, representing where the organism invaded blood vessels and caused infarctions. These ulceritic lesions are single or multiple and heal with scar formation. The mechanism of tissue destruction is Pseudomonas exotoxin A, a toxin similar to Corynebacterium diphtheriae toxin that causes inactivation of elongation factor 2, although sepsis resulting from other gram negative bacteria can also cause this condition.
EBV?
Infectious mononuclosis
Glandular fever
PTLD (post transplant lymphoproliferative disease)
Lymphoma
HIV related lymphoma
CMV?
Reactivation is common
disease is less common
distinguishing between them is hard
pneumonitis in transplant patients (associated with rejection and graft v host disease)
Retinitis and gastritis in HIV
name three most common protozoa?
Intracellular organisms
become a problem when CMI is affected (HIV, lymphoma)
Giardiasis
Cryptosporidiosis
Toxoplasmosis
