Compilation for Patients Diagnosed with UTI

Table 1: Suspected Organisms, Relevant tests and expected results of tests for respective patients diagnose with UTI

ABBREVIATIONSNA - Not applicable

REFERENCES1) Geo FB, Janet SB & Stephen AM. (2004). Jawetz, Melnick, & Adelberg’s Medical Microbiology. 23rd edition. McGraw-Hill.
2) Kenneth Todar. (2004). Staphylococcus. On site http://www.textbookofbacteriology.net

Protozoa diseases

In a place so hot and sweaty, the soldiers can easily get infected by these Protozoa;
Plasmodium, Giardia Lamblia, Crytosporidium and Entamoeba Histolytica.

Plasmodium
4 typical plasmodia that infects human includes: P. falciparum, P. vivax, P. malariae, P. ovale

Epidemiology
Generally limited to tropics and subtropics regions.
Relatively uncommon in the temperate zone, although epidemic outbreaks may occur when the largely nonimmune populations of these areas are exposed, usually unstable and relatively easy to control or eradicate.
Tropical malaria is usually more stable, difficult to control, and far harder to eradicate.

Mode of transmission
Transmission to humans occurs through the bite of female anopheles mosquitoes whereby sporozoites in mosquito saliva are injected into humans

Symptoms
-high fever
-chills
-muscle pain
-diarrhea

Clinical Findings
-Fever
Fever occurs and coincides with RBC lysis.
Periodic febrile episodes become obvious, coinciding with lysis of infected RBC.
Periodicity is 48 hours for P. falciparum, P. vivax, & P. ovale infection but 72 hours for P. malariae infection.

-Anemia
Anemia occurs as a result of RBC destruction leading to enlargement of liver and spleen.

-Large scale intravascular hemolysis
This is observed in P. falciparum infection. As a result, massive hemoglobinuria (blackwater fever) is observed due to the release of Hb from the RBC lysed intravascularly. Manifestation of intravascular hemolysis can include acute tubular necrosis and renal failure.

-Cerebral malaria
Cerebral malaria can result if P. falciparum malaria is left untreated.

Diagnosis
-Thick blood film
Microscopic examination of thick blood film stained with Giemsa’s stain at pH 7.2 helps demonstrates the presence of malarial parasites. This preparation concentrates the parasites and permits the detection even of the mild infections.

-Thin blood film
When the thick blood film demonstrates the presence of malarial parasites, further identification and confirmation of the specific malaria parasite could be done via performance of a Giemsa’s stained thin blood film that allows identification of characteristic specific to particular malaria parasites.
Chracteristics
P.falciparum has ring stage trophozoites that are small and is 1/5 of RBC diameter.
It also has 2 chromatin granules and crescentic gametocytes.
P.vivax has large rings that is ½ to 1/3 of RBC diameter and 1 chromatic granule. It has round or oval shape gametocytes.

-Serological methods
Polymerase Chain Reaction to detect Plasmodium nucleic acids or rapid diagnostic test employing the usage of dipsticks with monoclonal antibody specific against the target parasite antigen such as P. falciparum.

Prevention
-Chemoprophylaxis to travelers
-Mosquito net, window screens, protective clothing and insect repellents
-Drainage of stagnant water reduces the breeding areas

Treatment
Antimalarial grugs like Chloroquine. (1, 2)

Giardia Lamblia
Most common cause of waterborne epidemic diarrheal disease.
Common in wilderness areas because many animal carriers shed cysts into water.
Varies in severity

Mode of transmission
Parasitic in the intestines of humans and animals.
2 stages, one of which is a cyst form that can be ingested from contaminated water. Once the cyst enters the stomach, the organism is released into the gastrointestinal tract where it will adhere to the intestinal wall. Eventually the protozoa will move into the large intestine where they encyst again and are excreted in the feces and back into the environment. Once in the body, the Giardia causes giardiasis.

Symptoms
-Diarrhea
-abdominal cramps
-nausea
-weight loss
-general gastrointestinal distress.

Diagnosis
-Antigen testing of the stool. A small sample of stool is tested for the presence of Giardial proteins. The antigen test will identify more than 90% of people infected with Giardia.

-Can be diagnosed by examination of stool under the microscope; however, it takes three samples of stool to diagnose 90% of cases. Despite requiring three samples of stool, microscopical examination of stool identifies other parasites in addition to Giardia that can cause diarrheal illness. Therefore, microscopical examination of stool has value beyond diagnosing giardiasis, for example, it can diagnose other parasites as the cause of a patient’s illness.

-Collection and examination of fluid from the duodenum or biopsy of the small intestine, but these require a good deal of discomfort. The string test is a more comfortable method for obtaining a sample of duodenal fluid. For the string test, a gelatin capsule that contains a loosely-woven string is swallowed. One end of the string protrudes from the capsule and is taped to the patients outer cheek. Over several hours, the gelatin capsule dissolves in the stomach, and the string uncoils, with the last 12 inches or so passing into the duodenum. In the duodenum the string absorbs a small amount of duodenal fluid. The string then is untapped from the cheek and is removed. The collected duodenal fluid is expressed from the string and is examined under the microscope. Although more comfortable than some of the other tests, it is not clear how sensitive the string test is, for example, does it diagnose 60% (not very good) or 90% (very good) of cases of giardiasis.

Prevention
Avoiding contaminated water and the use of slow sand filters in the processing of drinking water

Treatment
Medicinally by quinacrine, metronidazole, and furazolidone. (3, 5, 6)

Cryptosporidium
Mode of transmission
Causes cryptosporidiosis. Spread by the transmission of oocysts via drinking water, which has been contaminated with infected fecal material. Oocysts from humans are infective to humans and many other mammals, and many animals act as reservoirs of oocysts, which can infect humans. Once inside of its host, the oocyst breaks, releasing four movable spores that attach to the walls of the gastrointestinal tract, and eventually form oocysts again that can be excreted.

Symptoms
-diarrhea
-headache
-abdominal cramps
-nausea
-vomiting
-low fever

Diagnosis
Polymerase Chain Reaction

Prevention
-Practice good hygiene
-Avoid water that might be contaminated
-Avoid food that might be contaminated.

Treatment
No treatment against the protozoa, patients will usually recover, but the disease can be fatal in late stage AIDS patients. (4, 5, 6)

Entamoeba histolytica
Mode of transmission
Via contaminated food and water
It is another water-borne pathogen that can cause diarrhea or a more serious invasive liver abscess. Ingested cysts excyst in the intestine and proteolytically destroy the epithelial lining of the large intestine.

Clinical Findings
May be asymptomatic to fulminating dysentery, exhaustive diarrhea, and abscesses of the liver, lungs, and brain.

Treatment
Several antibiotics

Prevention
Avoiding contaminated water, hyperchlorination or iodination can destroy waterborne cysts. (5, 6)

1. Brooks, G.F., Butel, J.S. & Ornston, L.N. (2004). "Jawetz, Melnick & Adeberg's Medical Microbiology", 23rd edition, Appleton & Lange.
2. http://health.yahoo.com/eney/healthwise/hw119119
3. http://www.medicinenet.com/giardia_lamblia/page3.htm
4. http://en.wikipedia.org/wiki/cryptosporidium
5. http://pages.cabrini.edu/sfuller-espie/Microbiology%20Lecture20Outlines/micro_fungal_protozoan_diseases.htm
6. http://udel.edu/

EMERGING AND RE-EMERGING INFECTIOUS DISEASES

Emerging infectious diseases are diseases of infectious origin whose incidence in humans have increased within the past decades or threatens to increase in the near future. The reappearance of a previously known infection after a period of disappearance or decline in incidence is known as re-emergence. Factors such as environmental degradation, rapid population growth, poverty, increased international travel, microbial adaptation of antibiotics, and development of insecticidal resistance and the collapse of public health systems may contribute to the emergence or re-emergence of a disease. Despite the discovery of antibiotics and vaccines, the world continues to be vulnerable to new, emerging, and re-emerging microbial diseases. New diseases in India include HIV/AIDS and a new strain of cholera (V. cholerae 0139) that emerged in 1992. Tuberculosis, malaria, dengue hemorrhagic fever and dengue shock syndrome, Japanese encephalitis, meningococcal meningitis, and hepatitis B .The outbreak of a plague epidemic in India in 1994 and the resurgence of Kala-Azar and epidemics of Leptospirosis are examples of the re-emergence of once-controlled infectious diseases. Preventive efforts and policies to ensure adequate supplies of appropriate medicines, and establishment of national and regional surveillance and diagnostic facilities for combating infectious disease threats should be established.Posted bymedical microbiologyat10:18 AM

Entamoeba histolytica

Several protozoan species in the genus Entamoeba infect humans, but not all of them are associated with disease. is well recognized as a pathogenic ameba, associated with intestinal and extra intestinal infections. The other species are important because they may be confused with E. histolytica in diagnostic investigations.
Life Cycle:
Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment. In many cases, the trophozoites remain confined to the intestinal lumen ( : noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients the trophozoites invade the intestinal mucosa ( : intestinal disease), or, through the bloodstream, extraintestinal sites such as the liver, brain, and lungs ( : extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E. histolytica and E. dispar. These two species are morphologically indistinguishable unless E. histolytica is observed with ingested red blood cells (erythrophagocystosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective).
Geographic Distribution:Worldwide, with higher incidence of amebiasis in developing countries. In industrialized countries, risk groups include male homosexuals, travelers and recent immigrants, and institutionalized populations.
Clinical Features:A wide spectrum, from asymptomatic infection ("luminal amebiasis"), to invasive intestinal amebiasis (dysentery, colitis, appendicitis, toxic megacolon, amebomas), to invasive extraintestinal amebiasis (liver abscess, peritonitis, pleuropulmonary abscess, cutaneous and genital amebic lesions).
Laboratory Diagnosis: must be differentiated from other intestinal protozoa including: E. coli, E. hartmanni, E. gingivalis, Endolimax nana, and Iodamoeba buetschlii (the nonpathogenic amebas); Dientamoeba fragilis (which is a flagellate not an ameba); and the possibly pathogenic Entamoeba polecki. Differentiation is possible, but not always easy, based on morphologic characteristics of the cysts and trophozoites. The nonpathogenic Entamoeba dispar, however, is morphologically identical to E. histolytica, and differentiation must be based on isoenzymatic or immunologic analysis. Molecular methods are also useful in distinguishing between E. histolytica and E. dispar and can also be used to identify E. polecki. Microscopic identification of cysts and trophozoites in the stool is the common method for diagnosing E. histolytica. This can be accomplished using:
§ Fresh stool: wet mounts and permanently stained preparations (e.g., trichrome).
§ Concentrates from fresh stool: wet mounts, with or without iodine stain, and permanently stained preparations (e.g., trichrome). Concentration procedures, however, are not useful for demonstrating trophozoites.
In addition, E. histolytica trophozoites can also be identified in aspirates or biopsy samples obtained during colonoscopy or surgery.
Diagnostic findings:
§ Microscopy
§ Immunodiagnosis
§ Molecular methods for discriminating between E. histolytica and E. dispar
§ Morphologic comparison with other intestinal parasites
§ Bench aid for E. histolytica

Treatment:For asymptomatic infections, iodoquinol, paromomycin, or diloxanide furoate (not commercially available in the U.S.) are the drugs of choice. For symptomatic intestinal disease, or extraintestinal, infections (e.g., hepatic abscess), the drugs of choice are metronidazole or tinidazole, immediately followed by treatment with iodoquinol, paromomycin, or diloxanide furoate



----------------------------------------------------------------------------------------------Posted bymedical microbiologyat8:53 PM

prion diseases

-AN OVERVIEW
Prince. C.P
Department of Microbiology
Mother Theresa Institute of Health Sciences
Puducherry

Infectious diseases are caused by microorganisms like bacteria, viruses, fungi, protozoan parasites and helminthic parasites.
Recent research by Stanley.B.Prusiner and others discovered the existence of a new group of infectious agents which are responsible for some rare fatal diseases. These agents do not belong to any of the classical pathogens, as they do not posses a nucleic acid (RNA/DNA) and are just infectious protein molecules. They are called as Prions.
Prions are small Self replicating proteinaceous infectious particles which can resist inactivation procedures like sterilization and can modify nucleic acids.
Prions are resistant to denaturation by proteases, heat, radiation, and formalin treatments, although their infectivity can be reduced by such treatments.
are often called Transmissible Spongiform Encephalopathies because of the post mortem appearance of the brain with large vacuoles in the cortex and cerebellum.
have Common features like long incubation periods (years), characteristic spongiform changes associated with neuronal loss and failure to induce inflammatory response-no antibodies are produced against prions.
in animals
Scrapie: sheep
TME (transmissible mink encephalopathy): mink
CWD (chronic wasting disease): mule -deer, elk
BSE (bovine spongiform encephalopathy): cows
in man
CJD: Creutzfeld-Jacob Disease
GSS: Gerstmann-Straussler-Scheinker syndrome
FFI: Fatal familial Insomnia
Kuru
Alpers Syndrome

These diseases are characterized by loss of motor control, dementia, paralysis, wasting and eventually death, typically following pneumonia.
The first Prion disease identified was Kuru, which was found among the Fore tribe of Papua New Guinea. .Kuru is transmitted among this tribe due to their practice of cannibalism .They eat their relative’s dead body.
Prion proteins induce abnormal folding of normal cellular Prion proteins (PrP) in the brain, leading to brain damage. When infectious PrP-sc enters into nervous tissues it interacts with normal PrP-c of the brain cells and converts them into Prp-sc. This leads into the accumulation of PrP-sc in brain cells.
Diagnosis is mainly based on symptoms. Other useful methods are 1.Electroencephalography — often has characteristic triphasic spikes
2. Cerebrospinal fluid analysis for 14-3-3 protein
3. MRI of the brain
No treatment is available today. The search for viable treatment is going on. Preventive measures like strict quarantine laws and mass slaughtering of infected animals are useful to control the spread of infection.
Prion research in future may provide the clarification for the doubts about origin of life and pathogenesis of diseases like Alzhmer’s and Parkinsonism.

-------------------------------------------------------------------------------------------------Posted bymedical microbiologyat10:32 AM

GLOBAL WARMING

WHAT IS ?
Carbon dioxide and other gases warm the surface of the planet naturally by trapping solar heat in the atmosphere. This is a good thing because it keeps our planet habitable. However, by burning fossil fuels such as coal, gas and oil and clearing forests we have dramatically increased the amount of carbon dioxide in the Earth’s atmosphere and temperatures are rising.
The vast majority of scientists agree that is real, it’s already happening and that it is the result of our activities and not a natural occurrence. The evidence is overwhelming and undeniable.
We’re already seeing changes. Glaciers are melting, plants and animals are being forced from their habitat, and the number of severe storms and droughts is increasing.
The number of Category 4 and 5 hurricanes has almost doubled in the last 30 years.
Malaria has spread to higher altitudes in places like the Colombian Andes, 7,000 feet above sea level.
The flow of ice from glaciers in Greenland has more than doubled over the past decade.
At least 279 species of plants and animals are already responding to , moving closer to the poles.
If the warming continues, we can expect catastrophic consequences.
Deaths from will double in just 25 years -- to 300,000 people a year.
Global sea levels could rise by more than 20 feet with the loss of shelf ice in Greenland and Antarctica, devastating coastal areas worldwide.
Heat waves will be more frequent and more intense.
Droughts and wildfires will occur more often.
The Arctic Ocean could be ice free in summer by 2050.
More than a million species worldwide could be driven to extinction by 2050.
There is no doubt we can solve this problem. In fact, we have a moral obligation to do so. Small changes to your daily routine can add up to big differences in helping to stop . The time to come together to solve this problem is now – TAKE ACTION
Posted bymedical microbiologyat9:19 AM

CHIKUNGUNYA VIRUS IN INDIA

Chikungunya is a relatively rare form of viral fever caused by an alpha virus (RNA Virus) that is spread by the bite of an infected Aedes aegypti mosquito. The virus is classified under arboviruses which are transmitted by arthropod vectors.

The name is derived from the Makonde word meaning “ that which bends up” in reference to the stooped posture developed as a result of the arthritic symptoms of the disease. The disease was first described in 1952 following an outbreak on the Makonde plateau along the border between Tanganyika and Mozambique.

Chikungunya virus was first isolated from Indian subcontinent in 1963 from Calcutta, since then there have been several reports of Chikungunya virus infection in different parts of India. The last outbreak of Chikungunya virus infection occurred in India in 1971. subsequently the virus had ‘disappreared’ from the subcontinent. However, recent reports of large scale outbreak of fever caused by Chikungunya virus infection in several parts of South India have confirmed the reemergence of this virus.

The symptoms of this infection include abrupt onset of fever, chills, headache and severe joint pain with or without swelling (usually the smaller joints), low back pain and rash. The symptoms are most often clinically indistinguishable from those observed in dengue fever. Therefore it is very important to clinically distinguish Dengue from Chikungunya virus infection. Unlike Dengue Hemorrhagic manifestations are relatively rare and as a rule shock is not observed in Chikungunya virus infection. Most often Chikungunya is a self limiting febrile illness. However, neurological complications such as meningoencephalitis and mother to child transmission has been observed.

The precise reasons for the reemergence of Chikungunya in the Indian subcontinent in not known. Although it is well recognized that reemergence of viral infection are due to a variety of social, environmental, behavioral and biological changes. The challenge faced during this large outbreak in the country has been the lack of rapid diagnostic facilities. Although, the National Institute of Virology at Pune, has been a great help in determining the etiology of the outbreak, relying on one institute in the country to render diagnostic help for case management would be a foolish task. It would be therefore desirable to ensure that several virology laboratories in the country are enrolled and networked to deliver rapid diagnosis in large outbreak such as this as well other emerging viral infections like Chandipura and Avian Influenza.

PRINCE.C.P
Lecturer in Microbiology
Posted bymedical microbiologyat12:21 AM