Question

Case Report #5 On July 4, 2007, Florida's Central District Health Department (CDHD) received a complaint of several ill persons with watery diarrhea after attendance at a municipal splash park on June 26. Water samples collected from splash features and an adjacent drinking fountain tested positive. The report by Florida Department of Health summarized the investigation of the outbreak and highlights the importance of splash park design, operation, access to hygiene facilities, and public education in prevention of waterbome parasites and other infectious agents. The exposures occurred at a recently constructed splash park located within a municipal park in a suburban community in Florida with a surrounding population of 550,000. Splash parks are increasingly popular venues associated with recreational water illness. The initial investigation by CDHD and CDC began on July 7 with interviews of 20 persons who attended a party at the splash park on June 26. Among those 20 persons, 12 reported gastrointestinal illness that began July 1-6 (6-11 days after exposure), including eight persons who reported watery diarrhea. All 12 ill persons reported exposure to splash-feature water, and six reported exposure to water from a nearby drinking fountain. No food items at the party were implicated as the source of the outbreak. Investigators hypothesized that swallowing contaminated splash park water was the source of illness. A clinical case was defined as the onset of diarrhea (three or more loose stools in 24 hours) or four or more symptoms consistent with gastroenteritis (i.e., abdominal cramps, nausea, vomiting, fever, or body aches) in a person within 1--12 days after visiting the municipal park. A confirmed case was defined as illness in a person with a positive IFA stool test result. Oocysts in stool specimens and molecular analysis of the specimens also gave positive test results. Watery diarrhea was the most frequent symptom, and in some patients was accompanied by dehydration, weight loss, abdominal pain, fever, nausea and vomiting. No hospitalizations or deaths associated with illness were reported The following topics should be answered. Type the question and then your answer under the question. 1. Introduce your disease. Include other names, history, researchers who studied it. 2. The microorganism that causes the disease (scientific name where appropriate) 3. Is the causative agent bacterial, viral, protozoan, parasitic (helminthes), or a fungal disease? 4. Characteristics of the microorganism; Shape; Genetic Material; Gram staining; acid fast staining; endospore forming, nutrition requirements; environmental conditions (ie, in which type of environment does the pathogen thrive (ie, oxygen, acid, salt) If your disease is caused by a virus for example, give an overview of its shape, nucleic acid etc. 5. How does the microorganism cause the disease? Elaborate on the disease. Which organ system is affected? 6. What are some of the symptoms of the disease? What would occur if there is worsening of symptoms? 7. What is the mode of transmission or source of the infection (how does a person become infected)? How would you confirm the disease (serum, antibodies, diagnostic test ets? Be specific)? 9. What medical treatment is recommended and appropriatte? 10. What else must be determined about the disease or your particular case study if you choose; (particulars about the patient history, source of infection, reoccurrence, risk of exposure, ctc) 11. Is this a nationally notifiable disease, or an emerging infectious disease? 12. What are some statistics of incidence and prevalence of this disease in certain areas of the world as reported by WHO? In the United States reported in MMWR by the CDC?? 13. Any other information you might find appropriate for your particular disease such as a case study (find on cdc.gov) and/or up to date research. 14. The last page of your paper should include "Reference page with resources cited.

Answer 1

1)Cryptosporidium infection (cryptosporidiosis) is an illness caused by tiny, one-celled cryptosporidium parasites. When cryptosporidia (krip-toe-spoe-RID-e-uh) enter your body, they travel to your small intestine and then burrow into the walls of your intestines. Later, cryptosporidia are shed in your feces.

In most healthy people, a cryptosporidium infection produces a bout of watery diarrhea and the infection usually goes away within a week or two. If you have a compromised immune system, a cryptosporidium infection can become life-threatening without proper treatment. You can help prevent a cryptosporidium infection by practicing good hygiene and avoiding swallowing water from pools, recreational water parks, lakes and streams.

2)Cryptosporidium parvum

Cryptosporidium parvum. Cryptosporidium parvum is one of several species that cause cryptosporidiosis, a parasitic disease of the mammalian intestinal tract.

3) Causative organism is parasite.

4) Shape: Endogenous developmental stages appear as small basophilic bodies (3-6µm) attached to the luminal surface of host epithelial cells; while exogenous oocysts appear as ovoid phase-bright ovoid bodies (5-7 x 4-6µm) containing four sporozoites and an eccentric residual body.

Morphology • Infective form- oocyst • Spherical, oval, 5um in diameter Does not stain with iodine and is acid fast Thick walled but 20%thin walled- autoinfection 4 crescent shaped sporozoites • Very hard and resistant. Temperature-60°C Sequential application of ozone and chlorine - eliminate cyst

A. Oocyst Morphological forms B. Sporozoites 1. Oocysts=infective stage 2. Sporozoites= infective and diagnostic -each contains one nucleus 3. Trophozoite 4. Type 1 meront 5. Type Il meront 6. Microgamont 7. Macrogamont A. B. w 4000 times bigger than normal

Parasite life cycle and biology

Sporulated oocysts, containing four sporozoites, are released from an infected host upon defecation. These environmentally resistant oocysts are encased in a durable oocyst wall; a complex protective barrier consisting of inner and outer oocyst walls composed of a protein-lipid-carbohydrate matrix . The infective cycle begins anew when an appropriate host ingests oocysts. The infectious dose varies depending on parasite isolate, yet as few as 10 oocysts have been reported to cause disease. Members of the genus Cryptosporidium complete all developmental stages in a single host . C. parvum oocysts excyst in the gastrointestinal tract, releasing four motile, infective sporozoites through a suture in the oocyst wall . Temperature and pH alone are sufficient to induce excystation , yet other environmental cues may include carbon dioxide, pancreatic enzymes, and bile salts . The excystation process also likely depends on parasite derived molecules including sporozoite-associated serine and cystine proteases , arginine aminopeptidase ,secretory phospholipase A2 ,and protein synthesis-associated molecules including ribosomal-associated and heat shock proteins . Through a mechanism of host cell attachment and subsequent invasion, a sporozoite is encapsulated by a parasite modified host membrane to form a parasitophorous vacuole, a structure common to apicomplexans. The parasitophorous vacuole of Cryptosporidium is unique in that it remains extracytoplasmic yet is considered intracellular as it maintains its position within the host derived parasitophorous vacuole membrane on top of epithelial cells. During internalization, a unique highly invaginated membrane, the feeder organelle, forms between the parasite and host cytoplasm. Localization studies have demonstrated that at least one of the parasite-derived ATP-binding cassette containing proteins, CpABC1, localizes to the feeder organelle and likely confers selective transport between host and parasite for nutrient uptake. The trophozoite undergoes asexual reproduction by merogony forming a Type-I meront. Cell division results in the formation of daughter cells, each surrounded by its own membrane, while still in the mother cell in a process known as endopolygeny. Under the current paradigm of C. parvum development, two developmentally distinct types of meronts are formed; Type-I and Type II .both produce merozoites, which are morphologically similar to sporozoites.

CDC SAFEREALTHIER PEOPLE http://www.dpd.cdc govidpdx Thick-walled oocyst ingested by host Drinking water Recreational water Contamination of water and food with oocysts 2 A-Infective Stage A Diagnostic Stage i 1 Thick-walled oocyst d (sporulated) exits host sporozoite Trophozoite Thick-walled Oocyst @ cocyst (sporulated) Type I Meront exits host Oly SVA 24 Auto-infection Asexual Cycle Thin walled ocyst (sporulated) Merozoite Microgamont Microgametes Und Merentiated Gamont Merz Type II Meront Sexual Cycle Macrogamon

5)

The mechanism by which Cryptosporidium causes diarrhea includes a combination of increased intestinal permeability, chloride secretion, and malabsorption, which are all thought to be caused by the host response to infection. In immunocompetent persons, the infection is usually limited to the small intestine.

As few as 2 to 10 oocysts can initiate an infection.The parasite is located in the brush border of the epithelial cells of the small intestine. They are mainly located in the jejunum. When the sporozoites attach the epithelial cells’ membrane envelops them. Thus, they are “intracellular but extracytoplasmic”.The parasite can cause damage to the microvilli where it attaches.The infected human excretes the most oocysts during the first week. Oocysts can be excreted for weeks after the diarrhea subsides from infections by C. parvum or C. hominis;however, immunocompetent individuals with C. muris infections have been observed excreting oocysts for seven months.

6)

The first signs and symptoms of cryptosporidium infection usually appear within a week after infection and may include:

• Watery diarrhea
• Dehydration
• Lack of appetite
• Weight loss
• Stomach cramps or pain
• Fever
• Nausea
• Vomiting

Worsening of symptoms may be characterised by severe signs of dehydration such as sunken eye balls, decreased skin turgor and hypovolemic shock.

7) Mode of transmission is mainly feco- oral route

Cryptosporidium infection begins when you ingest the one-celled cryptosporidium parasite. Some strains of cryptosporidium may cause more serious disease.

These parasites then travel to your intestinal tract, where they settle into the walls of your intestines. Eventually, more cells are produced and shed in massive quantities into your feces, where they are highly contagious.

You can become infected with cryptosporidia by touching anything that has come in contact with contaminated feces. Methods of infection include:

• Drinking contaminated water that contains cryptosporidium parasites
• Swimming in contaminated water that contains cryptosporidium parasites and accidentally swallowing some of it
• Eating uncooked, contaminated food that contains cryptosporidia
• Touching your hand to your mouth if your hand has been in contact with a contaminated surface or object
• Having close contact with other infected people or animals — especially their feces — which can allow the parasite to be transmitted from your hands to your mouth.

8)The simplest way to diagnose cryptosporidium infection is a method called an acid-staining test, which identifies cryptosporidium under a microscope. To obtain cells for the analysis, your doctor might ask for a stool sample, or in more extreme cases, take a tissue sample (biopsy) from your intestine for the test.

• Stool culture. Your doctor might also order a standard stool culture. Although this test cannot detect the presence of cryptosporidium, it may help rule out other bacterial pathogens.
• Other tests. Once it's clear that your infection is caused by cryptosporidium parasites, you may need further testing to check for development of serious complications. For example, checking liver and gallbladder function may determine whether the infection has spread. If you have both AIDS and cryptosporidiosis, a T-cell count — which measures the level of a certain white blood cell that's part of your immune system — can help predict the duration of the cryptosporidiosis. A T-cell count under 100 cells per microliter means you're more likely to have complications.

9)

• Anti-parasitic drugs. Medications, such as nitazoxanide (Alinia), can help alleviate diarrhea by attacking the metabolic processes of the cryptosporidium organisms. Azithromycin (Zithromax) may be given along with one of these medications in people with compromised immune systems.
• Anti-motility agents. These medications slow down the movements of your intestines and increase fluid absorption to relieve diarrhea and restore normal stools. Anti-motility drugs include loperamide and its derivatives (Imodium A-D, others). Talk with your doctor before taking any of these medications.
• Fluid replacement. You'll need either oral or intravenous replacement of fluids and electrolytes — minerals, such as sodium, potassium and calcium, that maintain the balance of fluids in your body — lost to persistent diarrhea. These precautions will help keep your body hydrated and functioning properly.
• Antiretroviral therapies. If you have HIV/AIDS, highly active antiretroviral therapy (HAART) can reduce the viral load in your body and boost your immune response. Restoring your immune system to a certain level may completely resolve symptoms of cryptosporidiosis.

10) Risk for exposure should be determined which is:

People who are at increased risk of developing cryptosporidiosis include:

• Those who are exposed to contaminated water.
• Children, particularly those wearing diapers, who attend child care centers.
• Parents of infected children.
• Child care workers.
• Animal handlers.
• Those who engage in oral-to-anal sexual activity.

11) Cryptosporidiosis is a nationally notifiable disease in United kingdom.

12)Prevalence rates reported in large-scale surveys of fecal oocyst excretion generally range from 1-3% in developed countries in Europe and North America.  Children, especially those younger than 2 years, appear to have a higher prevalence of infection than do adults.

Cryptosporidiosis is a notifiable disease at the European Union level, and surveillance data are collected through the European Basic Surveillance Network.  The crude incidence rate was similar to that in the United States, although considerable differences in the rates of cryptosporidiosis between countries were observed.A pronounced seasonal peak was observed in the autumn season, with 59% of cases reported between August and November. However, Ireland and Spain experienced a peak in spring and summer, respectively. Routine cryptosporidiosis surveillance in northwest England over 17 years revealed that cases predominantly occurred in spring and autumn. There, most infections are caused by C hominis, while C parvum is associated with rural areas and animal contact.

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