Pathogens L11-14
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Pathogens L11-14 - Leaderboard
Pathogens L11-14 - Details
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| Focus of control | Interrupt transmission by: controlling intra-domiciliary vectors in Latin America, screening blood transfusion in worldwide, screening organ transplantation, screening for congenital infection. |
| Insecticide and other control options | Insecticide impregnated materials: ITNs, IRS. House improvement: Plastering of walls. Social interventions: School teachers, community leaders, focus groups, meetings and house visits. Sustainability is a key parameter in community participation. Good practices’ may be acquired, but abandoned if regarded low priority. |
| Important vectors | Triatoma infestans: Domesticated vector. Rhodnius prolixus: Mostly peri-/domestic, some sylvatic populations. Prefers huts with palm-thatch roofs and peridomestic palms. Triatoma dimidiata: Sylvatic and domestic colonisers. Hides in dirt floors |
| Case study: Gran Chaco region | Argentina, Bolivia, Paraguay, 1.3 million km2, Indigenous communities, Highest transmission, House infestation 82–100%, T. infestans infection with T.cruzi, 50% |
| Bug re-invasion patterns as inferred from genetic studies | T. infestans and R. prolixus are domestic species across most of their ranges, so show low genetic diversity in natural populations and laboratory colonies. T. dimidiata and T. brasiliensis widespread across domestic, peri-domestic and sylvan habitats, generally show higher genetic diversity. |
| Wild T. infestans populations | Higher T. infestans genetic diversity in Bolivian Andes suggests: region of origin and geographic dispersal. Differences in the Andean as compared with non-Andean T. infestans populations. Associated with wild guinea-pigs and sylvatic cycle. Still limited gene flow between sylvatic and domestic populations |
| Insecticide control options- Triatomid resistance | Insecticide types: DDT not effective, organophosphates, synthetic pyrethroids, dieldrin, BHC, cypermethrin. Formulations: Wewtable powder and suspension concentrates, emulsifiable concentrates, microencapsulated formulations and insecticidal paint. |
| Transmission persistence in Gran Chaco | Inadequate insecticide spraying practices and formulations. Climate extremes degrade active insecticide molecule. Rapid household bug re-infestation after IRS. Wild T. infestans for reinvasion and maintaining genetic diversity. Lacks systematic surveillance and tools to monitor for re-infestation. Poor house construction. Lacks the political infrastructure and investment. |
| Apicomplexan structure | The 'apical complex' includes secretory organelles known as micronemes and rhoptries, polar rings composed of microtubules, and in some species a conoid which lies within the polar rings. At some point during their life cycle, members of the apicomplexa either invade or attach to host cells. It is during this invasive (and/or motile) stage that these apical organelles are expressed as well as the subpellicular membranes. |
| Apicomplexan Parasite | Apicomplexan parasites actively secrete proteins at their apical pole as part of the host cell invasion process in response to free Ca++ in the parasite's cytoplasm. When present the conoid is located in the center of the polar rings, with the short narrow end pointing anteriorly. The conoid intermittently protrudes beyond the apical end of the microtubules. Protrusion of the conoid is sensitive to parasite cytoplasmic calcium concentration. The rhoptries are club shaped secretory organelles, often located near the apical end of Apicomplexan intracellular parasites. Rhoptries are secreted during host cell invasion, and rhoptry proteins are found within the lumen and the membrane of very early stages of the forming parasitophorous vacuole. |
| Apicomplexan life-cycle | Sporogony: after asexual reproduction that produces sporozoites. Merogony: Sporozoites will undergo another asexual reproduction. Gametogony. |
| Malaria | Malaria is caused by five distinct Plasmodium species in humans: small subunit rRNA gene sequence similarity suggests more closely related to Plasmodium of other animals that to each other. The majority of morbidity and mortality is caused by P. falciparum. P. vivax with most morbidity caused in children under 10. Vector is female Anopheles mosquito. |
| Disease presentation | Asymptomatic malaria – circulating parasites but no symptoms. Uncomplicated malaria – nonspecific symptoms – fever, shaking chills, profuse sweating, headache, nausea, vomiting, diarhoea, anaemia. Complicated malaria – as above with additional organ damage and anaemia. Associated with hyperparasetemia and increased mortality. |
| Cause of disease symptoms | The blood-stage parasites within a host usually undergo synchronous schizogony. The simultaneous rupture of the infected erythrocytes and the release of antigens and waste products accounts for the intermittent fever associated with malaria occurring at either 48 or 72 hour intervals. |
| P. falciparum | P. falciparum causes cerebral malaria which is often fatal, extremely high temperature is associated with convulsions and coma. Infected erythrocytes adhere to capillary endothelial cells. Erythrocytes become knobbly, as a result of parasite proteins exported to the membrane, these bind to ligands on host cells. Blackwater fever: massive lysis of erythrocytes causes high levels of free haemoglobin in the blood and renal failure. |
| An arms race | The P. falciparum genome contains a large family of 60 var genes that encode hypervariable P. falciparum erythrocyte membrane protein 1 (PfEMP1). During the erythrocytic stage, each parasite expresses one of its var genes at a time. By switching between different var genes during the course of infection, the parasite is able to evade destruction by host immunity. P. vivax can only enter erythrocytes with genetically determined receptor sites known as Duffy blood groups. Sickle cell anaemia is protective against malaria; heterozygotes have some normal haemoglobin and have 80-95% protection against P. vivax. |
| Malaria diagnosis | WHO criteria : fever and presence of parasites. Light microscopic examination of a blood smear. Rapid diagnostic test. |
| Vector control - female anopheles | Widespread insecticide / larvicide. Destruction of breeding grounds. Indoor residual spraying. Long-acting insecticide treated bednets. Experimental approaches: – Endectocides (invermectin). – Sterile insect techniques. – CRISPR/CAS9 gene drives. – Wolbachia infection. |
| Insecticide-Treated Bed Nets | Reduce severe disease and mortality. Pyrethroid is approved for use. Long lasting insecticidal nets preferred. |
| Sterile insect techniques | Irradiated males. GM spermless males. Are not as competitive in mating flights. |
| Drugs for malaria prophylaxis | Kill parasite in the liver (casual). Kill asexual parasites in RBC (suppressive). Kill sexual parasites (gametocytocidal) |
| Chloroquine and the Food Vacuole | The food vacuole is a lysosome-like organelle in which the breakdown of hemoglobin and the detoxification of haeme occurs. Chloroquine concentrates up to several 1000-fold in the food vacuole of the parasite. |
| Factors that contribute to the increased risks of Cryptosporidium | Small size of oocysts. wide range of host specificity and monoxenous development. close associations between human and animal hosts. large number of oocysts excreted (up to 100 billion per calf). low infective dose. |
| Cryptosporidium in potable water - filtration | Sedimentation – because of small size and low density the settling rate of oocysts is extremely low and removal by sedimentation is insignificant. flocculation - clumping with -ve charged particles. rapid filtration - successful after flocculation. slow sand filtration - the top few centimetres support aerobic bacteria that produce a network of extracellular polymers forming a natural biological filter. membrane filtration - final finishing process. |
| Cryptosporidium in potable water - disinfection | Chlorination, UV light, Ozonisation |
| Therapy | No safe or effective therapy yet. Supportive case only treatment. Oral or intravenous rehydration is important. Spiramycin (macrolide antibiotic) has produced partial responses in patients but have no yielded reliability. Paromomycin decrease the intensity of infection and improve intestinal function and morphology. Nitoxazonide is partially effective in immuno-competent patients |
| Toxoplasmosis | T. gondii causes chronic infections in up to one-third of the human population and in animals. Healthy people causes mild symptoms, in unhealthy causes life threatening symptoms. complex life cycle consisting of intestinal and tissue phases. a typical intestinal life cycle consisting of merogony and gamogony. The sexual cycle produces oocysts which are excreted in the faeces. |
| Cycle | Intermediate hosts - ingestion of sporulated oocysts. Sporozoites are released, penetrate the intestinal epithelium, and invade macrophages and other types of cells. The parasite undergoes binary fission to form tachyzoites. The host cell will rupture and release the tachyzoites which will invade new host cells and repeat the replicative cycle. Infected macrophages will disseminate the tachyzoites throughout the host during this acute infection. |
| Route of human infection | Ingestion of contaminated materials and undercooked meats. Infections rates are 50% higher in cows, cattle and chickens. 38% of UK meat in +ve. Congenital transmission is only available in acute infection. |
| Dormant and Reactivation | As the host develops immunity the replication rate will slow and the infected host cells will become encapsulated. These slowly replicating forms are called bradyzoites and represent a dormant or resting stage. Bradyzoites secrete chitin and other components to form a cyst wall. The reactivation of infection is associated with waning immunity. Initiation of the tachyzoite stage of the infection is followed by local tissue damage and inflammation. Interferon γ is the essential mediator of the immune response, necessary to maintain latency. Cytokine production by microglia, astrocytes and neurons, which control inflammatory responses. |
| Symptoms and treatment | Early symptoms of toxoplasmic encephalitis include headache, fever, lethargy, and altered mental status with progression to neurological deficits and convulsions. The disease is almost always due to a reactivation of a latent infection and tends to remain confined to the CNS. The recommended treatment is the synergistic combination of pyrimethamine plus sulfadiazine. Interfere with folic acid synthesis by inhibiting the enzyme dihydrofolate reductase. Spiramycin for prophylactic use during pregnancy. |
| Fungi pathogens | Rigid Cell wall, chemoheterotrophs, saprophytes or parasites, recyclers, stimulate plant roots, infect skin, hair, nails. Asperigillus produce aflatoxin to cause liver cancer. Fungi fit into two Kingdoms: Chromistan - pseudofungi with cellulosic hyphal walls and Eumycotan - true fungi with chitinous hyphal walls. |
| Fungi cause disease through three major mechanisms | 1. Causing allergic reactions 2. Producing toxins and 3. By infection mycosis: growth in or on the body |
| Fungal infections (3 groups) | 1. Dermatophytes: attack outer surface of humans. 2. Soil organisms: thermal dimorphic saprobes. 3. attack when our defences are down - Opportunistic. |
| Three main types of human fungal infections | 1. Cutaneous - on skin 2. subcutaneous - on wounds 3. systemic mycoses - pathogenic or opportunistic saprobic fungi. |
| Ringworm | Infections are caused by 20 species of dermatophyte fungi grouped into 3 genera. Infections spread by direct or indirect contact with an infected individual or animal. Disease process is unique for two reasons: 1. no living tissue is involved 2. have evolved a dependency in humans and animals. |
| T. Pedis infections | Usually caused by the shedding of skin scales containing viable infectious hyphal elements of the fungus. Scales may remain infectious in the environment for months or years. Therefore transmission may take place by indirect contact long after the infective debris has been shed. Substrates like carpet and matting that hold skin scales make excellent vectors. |
| Treatment & Prevention of Tinea infections | Topical therapy for skin. Oral antifungals for scalp and nails. Fluconazole: bis-triazole antifungal agent, five membered ring containing three nitrogen atoms. inhibition of cytochrome P450 14ademethylase an enzyme in the sterol biosynthesis pathway that leads from lanosterol to ergosterol. |
| Yeasts | Unicellular, eukaryotic. Facultative anaerobes. Thich wall. Yeast Candida albicans form pseudohyphae, which elongate to form tubes which creates a fake mould. It helps to colonise deeper tissues. The pseudohyphae are dimorphic: yeast-like and mould like. It causes candidiasis: vaginitis, thrush, and balanitis. Oral candidiasis: white plaques, swollen gums. Diagnosis: microscopy, collecting samples. |
| Reproduction of yeasts | Yeasts reproduce asexually by a process called budding. Yeasts can also reproduce sexually by means of sexual spores called ascospores which result from the fusion of the nuclei from two cells followed by meiosis. |
| Treatment & Prevention of Candida infections | For cutaneous candidiasis control of excessive moisture, heat and friction which cause local skin maceration and treatment with a topical imidazole compound is usually effective. For oral candidiasis nystatin, amphotericin B or miconazole are effective. Azoles prevent the synthesis of ergosterol. Polyenes interfere with the integrity of the fungal cell membrane by binding to membrane sterols |