Clinical Immunology BMLS 3051 Lesson 9 Infectious Diseases PDF

CLINICAL IMMUNOLOGY BMLS 3051 Lesson #9:Infectious Diseases  Selected Infectious Diseases – Pathogens; clinical presentations and diagnostic aspects Corynebacterium –Clostridium tetatni diphtheriae Clostridium botulinum Trichophyton spp. Streptococcus Epidermophyton spp...

CLINICAL IMMUNOLOGY BMLS 3051 Lesson #9:Infectious Diseases  Selected Infectious Diseases – Pathogens; clinical presentations and diagnostic aspects Corynebacterium –Clostridium tetatni diphtheriae Clostridium botulinum Trichophyton spp. Streptococcus Epidermophyton spp. pyogenes Candida albicans Clostridium difficile Rabies virus Bacillus anthracis Hepatitis A virus (HAV) Vibrio cholerae Hepatitis B virus (HBV) Mycobacterium Hepatitis C virus (HCV) tuberculosis Human Papilloma Virus Entamoeba histolytic (HPV) Leishmania mexicana Neisseria meningitidis Trypanosoma cruzi Clostridium botulinum - Botulism Gram-positive, large, blunt-ended rods that produce endospores Most species are motile obligate anaerobe C. botulinum is found in soil and aquatic sediments. Its spores contaminate vegetables, meat, and fish. Botulism (food poisoning due to ingestion of exotoxin) and floppy baby syndrome C. botulinum colonizes the large intestine, producing exotoxin that is slowly absorbed. C. botulinum exotoxin inhibits the release of acetylcholine at the neuromuscular junctions, preventing contraction and causing flaccid paralysis, vomiting, and diarrhea. Lethargy, poor muscle tone Death can occur due to respiratory paralysis. Clostridium botulinum - Botulism Treatment: - Antitoxin (horse anti-serum) that neutralizes unbound botulinum toxin should be administered as soon as possible in suspected botulinal intoxication. Prevention: - Proper food preservation techniques prevent the production of the clostridial exotoxin Refrain from food products in cans that are swollen or dented especially those from places engaging in home – based canning and processing Clostridium tetani & Tetanus Clostridium tetani is a common soil bacterium and the causative agent of tetanus. Vegetative cells of C. tetani are gram positive rod-shaped. Tetanus: C. tetani spores infecting a puncture wound, a severe burn or postsurgical incision. fecal contamination of umbilical cord (neonatal tetanus) can occur also although rarely C. tetani exotoxin, tetanospasmin, binds irreversibly, penetrating neurons and blocking neurotransmitter release at inhibitory synapses. Specifically tetanus toxin gets transported in a retrograde way from the peripheral nervous system to the central nervous system by retrograde axonal transport. When tetanus toxin reaches inhibitory neuron terminals, it prevents the presynaptic release of inhibitory neurotransmitters glycine and gamma-aminobutyric acid (GABA). This causes severe, prolonged muscle spasms – spastic paralysis  Clostridium tetani & Tetanus In the early stages, the jaw muscles are affected, so that the mouth cannot open (trismusor “lockjaw”). Gradually, other voluntary muscles become involved. Death is usually the Lack of inhibitory signals to the motor result of paralysis of neurons and constant release of the chest muscles, acetylcholine (excitatory transmitter) to leading to the muscle fibers leads to irreversible respiratory failure contraction of the muscles and spastic paralysis. The muscle is too rigid and the patient can not move the muscle properly. It causes muscles to twitch uncontrollably or spasm.  Clostridium tetani & Tetanus – Common Clinical Presentations Patients have prolonged muscle spasms of both flexor and extensor muscles. Spastic muscle contractions, difficulty opening the jaw (called lockjaw, “trismus”), a characteristic smile called “risus sardonicus” and contractions of back muscles resulting in backward arching (Opisthotonos position). Patients are extremely irritable, and tetanic seizures develop, brought about by violent, painful muscle contractions following some minor stimulus, such as noise. Active immunization tetanus vaccine plays an essential role in preventing tetanus Treatment focuses on managing complications until the effects of the tetanus toxin resolve. Treatment will usually include antibiotics to kill bacteria and tetanus immune globulin (TIG) to neutralize the toxin already released. medicines may be necessary to control muscle spasms; ventilator may be required in really severe cases Entamoeba hystolytica- Amoebic dysentery 1) The pathogenic species for man is Entamoeba histolytica –e production of highly resistant, immotile cysts is one of the stages in the life cycle. Trophozoites are the actively feeding, reproductive (vegetative)stage Pathogenisis (Read): 1) Amoebic dysentery occurs when trophozoites of E. histolytica invade the walls of the large intestine and multiply in the submucosa, forming large flask- shaped ulcers. They ingest blood cells from damaged capillaries. It is usually less acute, lasts longer with no significant fever when compared to bacillary dysentery. 2) Amoebic Liver abscess occurs when E. histolytica amoebae that are carried to the liver via portal circulation, form abscess usually on the right lobe. This is more common in adult than children & in males more than females. Entamoeba hystolytica- Amoebic dysentery Host: Humans Transmission: fecal-oral (alimentary) Infective stage: mature cyst Localisation: large intestine Pathogenisis: 1) Intestinal amoebiasis: ingested cysts form trophozoites in the small intestines Pass to the colon’ feed on intestinal normal flora bacteria ,invade epithelium causing ulceration ulcers of the wall of the intestine, acute or chronic diarrhoea, stool containing blood and mucus; may be asymptomatic infection (Amoebic dysentery). 2) Extra- intestinal amoebiasis: abscess of liver, lung, brain, skin. Leishmania Mexicana – Cutaneous leishmaniasis (Bay sore; chiclero ulcer) Pathogen: Leishmania mexicana; L. tropica Leishmania braziliensis (subphylum Mastigophora – flagellates) Disease: Cutaneus leishmaniasis; Mucocutaneous Leishmaniasis (local: espundia) Geographical distribution: Central America, South America, Africa. Different type of Leishmaniasis (visceral)in Asia and Europe In Belize: North of Belize District; Cayo and southern Belize – seen especially among folks living in and or working in densely forested areas - loggers; soldiers; Forestry Dept personnel Transmission: by sand fly vector – Phlebotomus or Lutzomyia genra Hosts: man, dogs, wild rodents Localisation: cells of skin Leishmania Mexicana – Cutaneous leishmaniasis (Bay sore; chiclero ulcer) Trypanosoma cruzi – Chagas disease (American Trypanosomiasis) Pathogen: Trypanosoma cruzi Disease: American trypanosomiasis, or Chagas disease Geographical distribution: South and Central America Vector: 1) Infected bug species of the family Triatomidae; Reduviid – the are nocturnal Other mode of transmission: 1. congenital; 2. by blood transfusion. Reservoir hosts: armadillos, opossums, rodents, monkeys, dogs, cats. Localisation: blood (in acute Triatoma dimidiata – vector phase), cells of lymph nodes, commonly found in Belize spleen, liver, brain, muscles. Trypanosoma cruzi – Chagas disease (American Trypanosomiasis) ► From the site of bite wound (break in skin) or conjunctiva, trypanosomes from the insect’s feces reach the blood and lymphatics where they multiply. ► Acute phase is usually asymptomatic. But when symptomatic the patient suffers from fever, rash, headache, lymphadenopathy, oedema of the brain. There may be a Romania sign (Chagoma) swelling around the eyes ► There are alternating periods of fever and apparent recovery. This is followed by depression and progressive lethargy. ► The disease becomes chronic and persists for months and even years resulting in enlargement of the heart (cardiomegaly or dilated cardiomyopathy) and esophageal complications ► Diagnosis – serological methods to detect presence of antibodies ► Xenodiagnosis using “clean’ laboratory – bred triatomine bugs Trypanosoma cruzi – Chagas disease (American Trypanosomiasis) ► From the site of bite wound (break in skin) or conjunctiva, trypanosomes from the insect’s feces reach the blood and lymphatics where they multiply. ► Acute phase is usually asymptomatic. But when symptomatic the patient suffers from fever, rash, headache, lymphadenopathy, oedema of the brain. There may be a Romania sign (Chagoma) swelling around the eyes ► There are alternating periods of fever and apparent recovery. This is followed by depression and progressive lethargy. ► The disease becomes chronic and persists for months and even years resulting in enlargement of the heart (cardiomegaly or dilated cardiomyopathy) and esophageal complications ► Diagnosis – serological methods to detect presence of antibodies ► Xenodiagnosis using “clean’ laboratory – bred triatomine bugs THANK YOU