It’s almost the end of the semester, we have two more weeks of lectures and tests before we have one week of revision and then… exams! ><
Any who, today I will be doing a post for you all to practice on reading some patient and donor cards. As always, the answers will be at the bottom of the post 🙂
Oh and the featured image of this post is what we do in our lab! I love how this specialisation requires order, neat and structured work. Cleanliness is my jam.
ABO + Rh D (Patients)
- What are their ABO groups?
(with regards to Tran Song Lum, his serum was showing fibrin clots as it was an old serum sample from the university and is not actually an anomaly)
Antibody Screen + Antibody Panel
- What antibody does the patient have based on his panel? (You can find an empty ID panel to work this out on here)
Phenotyping Donors and Patient
- What are the phenotypes of the patient and donors?
- What is the patients Rh genotype (either in Fisher-Race or Wiener) ?
- Is Tran Song Lum’s antibody a result of an allo-antibody or an auto-antibody?
- Based on all the results gathered so far, do you expect any of the donors to be compatible with Tran Song Lum?
(If you were wondering why Donor 3 is missing it’s because I have already selected 4 donors who are also D negative and compatible with the patient according to their blood group which we tested for in tubes)
ABO + Rh D Patients
- Tran Song Lum – A Rh D Neg
- 4360507 – O Rh Pos
- 4360513 – O Rh Neg
- 4079107 – O Rh Pos
- 4360532 – A Rh Pos
- The patient had Anti-E
- The patient and all donors except for donor 5 are dCe/dce (or r’r)
- Donor 5 is dce/dce (or rr)
- The patient’s Anti-E is a result of an allo-antibody as he does not have the E antigen (as shown in his phenotyping card)
- Based on all the results, the donors should be compatible with the patient and crossmatch negative when performed by IAT.
Hi guys, its been a long time since I did a post on any organisms (will also try to get a post up on Transfusion soon). I’ve decided to do a post on amoeba’s since we just learnt them today and they’re fresh on my mind 🙂
Amoeba’s are a class of Protozoa. Protozoa are unicellular, eukaryotic organisms. Their cytoplasm is composed of an outer layer and an inner layer. The outer layer is called the ectoplasm and is gel like whereas the inner layer (endoplasm) is more liquid like.One species in particular Entamoeba histolytica (E. histolytica) is a human pathogen.
Entamoeba histolytica / dispar
Morphologically speaking, E. histolytica and E. dispar are very similar and cannot be distinguished so I have categorised them together. However, E. dispar is not pathogenic to humans.
E. histolytica causes amoebiasis and has a higher incidence in tropical areas but infections are distributed worldwide. Around 10% of the entire world is infected with this organism and guess what, its estimated that for every person infected, there are another 10-20 more people that are asymptomatic carriers (that’s a whoooole lotta people) !
Infections are usually associated with poor sanitation and developing areas. Humans are the reservoir host and can transmit infections to other humans and animals (dogs, cats, pigs, primates). They are transmitted mainly via the faecal-oral route, especially from asymptomatic individuals and food handlers that contain cysts. Other possible transmission methods is venereal (sexual transmission). The organism can reside harmlessly within the large intestine but they can colonize and penetrate the intestinal tissue, resulting in ulcers. They can then metastasize to other organs.
There is no intermediate host and infection occurs by ingesting a mature cyst. The cyst is resistant to environmental conditions and act as the reproducing and transmitting agent. The cyst becomes active when it reaches the lower small intestine as the pH is more neutral / alkaline compared to the stomach. One amoeba containing 4 cystic nuclei emerges, undergoes mitosis and gives rise to 8 small uninucleated metacystic trophozoites. They mature as they reach the large intestine and usually colonize at the caecum where conditions are favourable.When the trophozoites are in the intestinal lumen, they begin the path of passing out of the body. If this passage is not rapid (stool is formed), only cysts will be seen in the stool during diagnosis. If the passage is rapid (stool is diarrhoeal), then trophozoites will be seen as they haven’t begun forming into cysts yet.
Intestinal disease with a variable incubation period (few days – weeks – months). People that are asymptomatic do not show occult bleeding in their stools but do excrete cysts (no tissue invasion). E. histolytica can cause amoebic dysentery – which is acute diarrhoea with ulcers on the mucosal surface of the colon. The ulcers are flask shaped, with a narrow opening and ballooned area below the surface that is filled with pus. Symptoms are:
- lower abdominal pain
- frequent bowel movements
- electrolyte imbalance
- and in severe cases, blood diarrhoea
Patient’s can also present with amoebic colitis – the chronic form which has similar symptoms but with alternating periods of constipation over a long course. If the infection metastasizes, the most common organ that is next affected is the liver. This results in amoebic abscesses in the liver and symptoms include right abdominal pain, fever, sweating, weakness, weight loss, cough, haepatomegaly and jaundice may also be present. Cutaneous lesions can also be affected (i.e. the skin around the anus), which is especially seen in toddler’s when the stool may be in contact with the skin for longer periods of time. The other form of disease is amoeboma – a growth of granulomatous tissue which results in a large local lesion in the bowel that resembles carcinoma.
Below are some photos I took during my lab today of Amoebae. However they aren’t E. histolytica and are non-pathogenic. With the exception of Giardia lamblia which is a flagellate and can cause Giardiasis.
Below are just some photos I took last week when reading some of the results for 4 unknown organisms. I didn’t manage to take a photo of the yeast cells under the light microscope because I couldn’t align my camera to the optical eye piece 😦
We will be discussing our choice of tests and what organisms they were tomorrow, eek! Wish me luck, I already know I got one incorrect.
For those of you that noticed that a antimicrobial plate is missing for Unknown A, it’s because that was a yeast (I’m suspecting Candida based on my results) so there was no need to perform any antimicrobial resistance as it is of course, not a bacteria. The zone of no growth is measured with a ruler and there are set measurements for each specific antibiotic and its concentration that determine if an organism is susceptible or not, even though there is a clearing it needs to be of a certain diameter so its important to measure accurately!
Hi guys! I have an interesting organism today 🙂
The organism I will be doing a post on today is quite famous in the microbial world because of its history. I don’t usually mention the history of the organism’s in my post but I will briefly mention it here. During an American Legion convention in Philadelphia in 1976, 200 people contracted a severe multi-system disease that included pneumonia. Off the 200 affected, 29 people eventually died from this disease. It was later found to be caused by Legionella pneumophila (L. pneumophila) which resided in the hotel’s air conditioning system.
In this post I will be showing the practice cases that we had performed so that we could familiarise ourselves with the procedures on a transfusion reaction investigation in NZ. During our lab, we were given two patients that had shown clinical symptoms during a transfusion reaction, resulting in an investigation to determine if it was due to something serious aka ABO incompatible.
Last week, we got to experience for the first time, something that we would eventually do a lot of in Microbiology labs – sellotape flag mounts.
We also got to do a slide culture of Cladosporium (I have a photo of this guy at the bottom of my post), which we can observe in about 3 weeks time. Preparing a slide culture was super fun (and easy!). In this post I will be talking about how to perform the above techniques.