What is the difference between infected and infectious in epidemiology?

What is the difference between infected and infectious in epidemiology?

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I am studying the SIR model and in the infected class I, both infectious and infected individuals are included, as stated here

I know that the model uses the assumption that the disease has an insignificant incubation period so infected individuals are capable of transmitting the disease as soon as they become infected. But what is the specific difference between these two terms? Does infective mean anything different?

(The document you link to says "see Chap. 1 for distinction between infected and infectious individuals", but I'll assume you don't have access to that - I certainly don't.)

Infected individuals have been infected by a pathogen. Infectious individuals have the potential to transmit a pathogen to others.

Note that the definition given for "infected" in the source you link to is actually wrong: hosts may have a subclinical infection, in which case they are not "now sick with it".

Secondary infection

invasion and multiplication of microorganisms in body tissues, as in an infectious disease. The infectious process is similar to a circular chain with each link representing one of the factors involved in the process. An infectious disease occurs only if each link is present and in proper sequence. These links are (1) the causative agent, which must be of sufficient number and virulence to destroy normal tissue (2) reservoirs in which the organism can thrive and reproduce for example, body tissues and the wastes of humans, animals, and insects, and contaminated food and water (3) a portal through which the pathogen can leave the host, such as the respiratory tract or intestinal tract (4) a mode of transfer, such as the hands, air currents, vectors, fomites, or other means by which the pathogens can be moved from one place or person to another and (5) a portal of entry through which the pathogens can enter the body of (6) a susceptible host. Open wounds and the respiratory, intestinal, and reproductive tracts are examples of portals of entry. The host must be susceptible to the disease, not having any immunity to it, or lacking adequate resistance to overcome the invasion by the pathogens. The body responds to the invasion of causative organisms by the formation of antibodies and by a series of physiologic changes known as inflammation .

The spectrum of infectious agents changes with the passage of time and the introduction of drugs and chemicals designed to destroy them. The advent of antibiotics and the resultant development of resistant strains of bacteria have introduced new types of pathogens little known or not previously thought to be significantly dangerous to man. A few decades ago, gram-positive organisms were the most common infectious agents. Today the gram-negative microorganisms, and Proteus, Pseudomonas, and Serratia are particularly troublesome, especially in the development of hospital-acquired infections. It is predicted that in future decades other lesser known pathogens and new strains of bacteria and viruses will emerge as common causes of infections.

The development of resistant strains of pathogens can be limited by the judicious use of antibiotics . This requires culturing and sensitivity testing for a specific antibiotic to which the identified causative organism has been found to be sensitive. If the patient has been receiving a broad-spectrum antibiotic prior to culture and sensitivity testing, this should be discontinued as soon as the specific antibiotic for the organism has been found. It would be helpful, too, if the general public understood that antibiotics are not cure-alls and that there is danger in using them indiscriminately. In some instances an antibiotic can upset the normal flora of the body, thus compromising the body's natural resistance and making it more susceptible to a second infection ( superinfection ) by a microorganism resistant to the antibiotic.

Although antibacterials have greatly reduced mortality and morbidity rates for many infectious diseases, the ultimate outcome of an infectious process depends on the effectiveness of the host's immune responses . The antibacterial drugs provide a holding action, keeping the growth and reproduction of the infectious agent in check until the interaction between the organism and the immune bodies of the host can subdue the invaders.

Intracellular infectious agents include viruses, mycobacteria, Brucella, Salmonella, and many others. Infections of this type are overcome primarily by T lymphocytes and their products, which are the components of cell-mediated immunity . Extracellular infectious agents live outside the cell these include species of Streptococcus and Haemophilus. These microorganisms have a carbohydrate capsule that acts as an antigen to stimulate the production of antibody, an essential component of humoral immunity .

Infection may be transmitted by direct contact, indirect contact, or vectors. Direct contact may be with body excreta such as urine, feces, or mucus, or with drainage from an open sore, ulcer, or wound. Indirect contact refers to transmission via inanimate objects such as bed linens, bedpans, drinking glasses, or eating utensils. Vectors are flies, mosquitoes, or other insects capable of harboring and spreading the infectious agent.

Patient Care . Major goals in the care of patients with threatening, suspected, or diagnosed infectious disease include the following: (1) prevent the spread of infection, (2) provide physiologic support to enhance the patient's natural curative powers and resources for warding off or recovering from an infection, (3) provide psychologic support, and (4) prepare the patient for self-care if this is feasible.

Special precautions for prevention of the spread of infection can vary from strict isolation of the patient and such measures as wearing gloves, mask, or gown to simply using care when handling infective material. No matter what the diagnosis or status of the patient, handwashing before and after each contact is imperative.

Unrecognized or subclinical infections pose a threat because many infectious agents can be transmitted when symptoms are either mild or totally absent.

In the care of patients for whom special precautions have not been assigned, gloves are indicated whenever there is direct contact with blood, wound or lesion drainage, urine, stool, or oral secretions. Gowns are worn over the clothing whenever there is copious drainage and the possibility that one's clothes could become soiled with infective material.

When a definitive diagnosis of an infectious disease has been made and special precautions are ordered, it is imperative that everyone having contact with the patient adhere to the rules. Family members and visitors will need instruction in the proper techniques and the reason they are necessary.

Physiologic support entails bolstering the patient's external and internal defense mechanisms. Integrity of the skin is preserved. Daily bathing is avoided if it dries the skin and predisposes it to irritation and cracking. Gentle washing and thorough drying are necessary in areas where two skin surfaces touch, for example, in the groin and genital area, under heavy breasts, and in the axillae. Lotions and emollients are used not only to keep the skin soft but also to stimulate circulation. Measures are taken to prevent pressure ulcers from prolonged pressure and ischemia. Mouth care is given on a systematic basis to assure a healthy oral mucosa.

The total fluid intake should not be less than 2000 ml every 24 hours. Cellular dehydration can work against adequate transport of nutrients and elimination of wastes. Maintenance of an acid urine is important when urinary tract infections are likely as when the patient is immobilized or has an indwelling urinary catheter. This can be accomplished by administering vitamin C daily. Nutritional needs are met by whatever means necessary, and may require supplemental oral feedings or total parenteral nutrition . The patient will also need adequate rest and freedom from discomfort. This may necessitate teaching her or him relaxation techniques, planning for periods of uninterrupted rest, and proper use of noninvasive comfort measures, as well as judicious use of analgesic drugs.

Having an infectious disease can alter patients' self-image, making them feel self-conscious about the stigma of being infectious or &ldquodirty,&rdquo or making them feel guilty about the danger they could pose to others. Social isolation and loneliness are also potential problems for the patient with an infectious disease.

Patients also can become discouraged because some infections tend to recur or to involve other parts of the body if they are not effectively eradicated. It is important that they know about the nature of their illness, the purposes and results of diagnostic tests, and the expected effect of medications and treatments.

Patient education should also include information about the ways in which a particular infection can be transmitted, proper handwashing techniques, approved disinfectants to use at home, methods for handling and disposing of contaminated articles, and any other special precautions that are indicated. If patients are to continue taking antibacterials at home, they are cautioned not to stop taking any prescribed medication even if symptoms abate and they feel better.

1. Introduction

Seasonal infections of humans range from childhood diseases, such as measles, diphtheria and chickenpox, to faecal–oral infections, such as cholera and rotavirus, vector-borne diseases including malaria and even sexually transmitted gonorrhoea (Hethcote & Yorke 1984). Despite the near ubiquity of this phenomenon, the causes and consequences of seasonal patterns of incidence are poorly understood.

This paper examines these causes and consequences, providing an overview of seasonal infectious disease epidemiology. It is divided into three sections. In the first section, the causes of seasonal patterns of human infectious disease incidence and their association with different modes of transmission are briefly reviewed. The second section provides an overview of seasonal infectious disease epidemiology, examining the consequences of seasonality for threshold parameters, such as R0, disease outbreaks, endemic dynamics and persistence. The third section deals with the implications of seasonality for disease control by routine and pulse vaccination programmes. In the second and third sections, several new results are obtained concerning the expected size distribution of disease outbreaks and pulse vaccination strategies for seasonal infections. These results are discussed and areas for further empirical and theoretical work identified.


Data sources

Two hundred and fifty-three patients were enrolled in the prospective study [ Reference Mailles and Stahl 1]. According to the case definition, patients were aged ≥28 days, lived in mainland France, were hospitalized in public hospitals, were negative for HIV, and had remained in hospital for ≥5 days for surviving patients. The collected data included demographical and clinical features, and the causative agent when identified. The data was processed with Stata v. 11 (StataCorp., USA). The PMSI is a national exhaustive hospital discharge database implemented in 1997, which describes public and private hospital activity in France. For each hospitalization, the diagnoses are included in the database according to the World Health Organization (WHO) International Classification of Diseases codes, 10th revision, 2007 version (ICD-10-2007). Demographical data (age, sex), length of stay, hospital location, and death occurring during hospitalization are also recorded.

We selected records in the PMSI using criteria closely matching the case definition used in the prospective study:

• Patients aged ≥28 days, hospitalized in mainland France from January 1 to December 31 2007 in a public hospital.

• An encephalitis-associated hospitalization was defined as a hospitalization for which at least one of the ICD-10-2007 codes for encephalitis was listed as a discharge diagnosis (main, related, or secondary). The ICD-10-2007 codes for encephalitis used to select the records are listed in Table 1.

Table 1. List of diagnostic codes in ICD-10-2007 used for extraction of encephalitis cases

Patients with multiple hospitalizations were detected using their unique identifier and only data from the first hospitalization was taken into account.

Patients matching the following criteria were excluded to maintain comparability between hospital discharge data and the prospective study:

• surviving patients with a hospital stay <5 days,

• any ICD-10-2007 code consistent with HIV infection (R75, Z21, B20–B24, F024) on the patient's file,

• codes for intracranial abscess (G06, G07), prion diseases (A810), and cerebral malaria (B500) on the patient's file.

Furthermore, if hospitalization with an unexplained or unspecified encephalitis code (Table 1) was associated with any other code consistent with encephalitis-like diseases, the patient was excluded. Toxic (G92, F10–F16, F18, F19, T40–T44) autoimmune (G35–G37, G04.0, M30–36, D86), metabolic (G40.5, E05, E10.0), vascular (G43, G45, G46, I60, I63–I68), neoplasic (C79.3, C70–C72), psychiatric (F28, F29), and congenital (G80, G60, G10–13) diseases were considered as potential encephalitis mimickers. When an encephalitis-associated code appeared in the secondary diagnosis, the patient was included if the main discharge diagnosis was related to encephalitis (compatible symptom or complication) for example, main diagnosis R40 (somnolence, stupor, and coma), and secondary diagnosis B00.4 (herpes viral encephalitis).

Incidence was calculated by using the number of inhabitants in mainland France in 2007, as estimated by the National Institute of Statistics and Economic Studies, which has responsibility for the national census.

Causes of encephalitis

Aetiological agents were determined in the PMSI, using specific infectious encephalitis codes when defined in ICD-10-2007 (e.g. B02.0 zoster encephalitis). Some pathogens did not have any specific encephalitis code in ICD-10-2007, such as Mycoplasma pneumoniae or cytomegalovirus. In this case, the aetiological agent was kept for the diagnosis if one code listed in Table 2 (in the main, related or secondary diagnosis) was associated with a code for unspecified or unexplained encephalitis aetiology (Table 1).

Table 2. List of diagnostic codes in ICD-10-2007 used for aetiological identification when unknown causes code of encephalitis was extracted

We classified acute encephalitis hospitalizations collected from the PMSI by known cause or unknown cause and compared them with the prospective study's results.

Diagnosis in the PMSI are coded as primary diagnosis, related diagnosis (‘medical condition related to primary diagnosis’) or ‘associated’ (secondary) diagnosis (‘any medical condition that is relevant to primary diagnosis’). Within the PMSI, we compared the main characteristics of patients with primary or related diagnosis, to those of patients with secondary diagnosis.


Encephalitis-associated cases were processed using Stata statistical software, v. 11 (StataCorp.) and sorted according to aetiology, age, gender, district of residence, duration of hospital stay, and death during hospitalization. We compared all encephalitis cases and aetiological groups in the prospective study and PMSI using two-sided t tests or non-parametric tests for continuous variables and χ 2 or Fisher's exact test for categorical variables. Comparisons were assessed for statistical significance at P= 0·05.

Differences between infectious disease events in first liver transplant versus re-transplantation in the Swiss Transplant Cohort Study

Background & aims: Re-transplantation after graft failure is increasingly performed, but inferior graft survival, patient survival and quality of life has been reported. The role of infectious disease (ID) events in this less favorable outcome is unknown.

Approach & results: We analyzed ID events after first liver transplantation (FLTpx) and re-transplantation (re-LTpx) in the Swiss Transplant Cohort Study. Clinical factors were compared after FLTpx and re-LTpx, survival analysis was applied to compare the time to ID events after FLTpx and after re-LTpx, adjusted for age, gender, MELD score, donor type, liver transplant type (whole vs. split liver) and duration of transplant surgery. In total, 60 patients were included (65% male, median age of 56 years). Overall, 343 ID events were observed, 204 (59.5%) after the FLTpx and 139 (40.5%) after re-LTpx. Bacterial infections were most frequent (193/343, 56.3%), followed by viral (43/343, 12.5%) and fungal (28/343, 8.2%) infections, with less infections by Candida spp. but more by Aspergillus spp. after re-LTpx (P-value = 0.01). The most frequent infection site was bloodstream infection (86, 21.3%), followed by liver and biliary tract (83, 20.5%) and intraabdominal (63, 15.6%) infections, After re-LTpx, more respiratory tract and surgical site infections were observed (P-value < 0.001). The time to first infection was shorter after FLTpx (adjusted hazard ratio (HR) = 0.5 [confidence interval: 0.3, 1.0], p = 0.04). Reduced hazards for ID events after re-LTpx were also observed when modelling recurrent events (adjusted HR = 0.5 [0.3, 0.8], P-value = 0.003).

Conclusions: The number of infections was comparable after FLTpx and re-LTpx, however, differences regarding infection sites and fungal species were observed. Hazards were reduced for infection after re-LTpx.

Keywords: infectious complications liver re-transplantation organ allocation pre-transplant counseling prediction of infectious risks.


Rickettsiae microorganisms appear to exert their pathologic effects by adhering to and then invading the endothelial lining of the vasculature within the various organs affected. The adhesins appear to be outer membrane proteins that allow the rickettsia to be phagocytosed into the host cell. Once inside, the rickettsial organisms either multiply and accumulate in large numbers before lysing the host cell (typhus group) or they escape from the cell, damaging its membrane and causing the influx of water (spotted fever group). [4]

Rickettsiae rely on the cytosol of the host cells for growth. To avoid phagocytosis within the cells, they secrete phospholipase D and hemolysin C, which disrupt the phagosomal membrane, allowing for rapid escape.

The most important pathophysiologic effect is increased vascular permeability with consequent edema, loss of blood volume, hypoalbuminemia, decreased osmotic pressure, and hypotension. On the other hand, disseminated intravascular coagulation is rare and does not seem to contribute to the pathophysiology of rickettsiae.

Studies of murine models have demonstrated that rickettsiae are cleared by cytotoxic CD8 cells and by cytokine-activated rickettsicidal nitrogen and oxygen species. In fact, antibodies do not play an important role in immunity against pathogenic rickettsia upon fist exposure. Walker provided an excellent review of this topic. [1]

RMSF: In RMSF, rickettsiae multiply within the endothelial cells of small blood vessels and then gain access to the bloodstream after skin inoculation. Focal areas of endothelial proliferation and perivascular mononuclear cell infiltration cause leakage of intravascular fluid into tissue space. These vascular lesions can affect all organs however, they most readily are found in the skin and adrenals. In the central nervous system and heart, a damaging host response (primarily cell-mediated) accompanies the vasculitis. The liver is usually affected with portal triaditis. Vascular wall destruction consumes platelets, causing thrombocytopenia. Multiple factors lead to hypoalbuminemia (eg, renal loss, decreased intake, hepatic involvement) and hyponatremia (eg, renal loss, extracellular fluid shifts, cellular exchange of sodium for potassium).

Rickettsialpox: The organism that causes this illness is known to cause angiitis similar to other rickettsiae. Biopsies, which are rarely needed to establish the diagnosis of rickettsialpox, show evidence of thrombosis and necrosis of capillaries, as well as perivascular mononuclear cell infiltration.

Boutonneuse fever: Features of this illness are related to involvement of the vascular structures of the dermis in a manner similar to that observed in RMSF. Endothelial cells of the capillaries, venules, and arterioles (ie, small-to-medium sized vessels) in various organs may also become involved as the organism disseminates. [10] Additionally, a few cases of leukocytoclastic vasculitis have been reported with this infection.

Louse-borne (epidemic) typhus: The pathology is similar to that described for the spotted fever group of rickettsial diseases. However, typhus group rickettsiae do not stimulate actin-based mobility and rather extensively multiply and accumulate intracellularly until they burst the endothelial cell and disseminate into the bloodstream.

Brill-Zinsser disease (ie, relapsing louse-borne typhus): The pathology is similar to that described for the spotted fever group of rickettsial diseases. However, the organisms appear to lie dormant, most likely in the cells of the reticuloendothelial system, until they are reactivated by an unknown stressor, multiply and cause another acute but milder infection.

Murine (endemic or flea-borne) typhus: Pathology is similar to that described for epidemic typhus.

Tsutsugamushi disease (ie, scrub typhus): After invading the host cell and replicating in its cytoplasm, the Orientia tsutsugamushi exits by budding enveloped by part of the host cell membrane as it invades adjacent cells. Perivasculitis of small blood vessels occurs similarly to other rickettsial diseases. Usually, a necrotic inflammatory skin lesion occurs at the mite bite site, and regional and generalized lymphadenopathy is associated with this infection.

Q fever: In Q fever, the Coxiella organism directly causes disease in various organs. It has been demonstrated in macrophages in the lungs and in vegetations of the heart valves. Host-mediated pathogenic mechanisms also appear to play an important role in disease pathogenesis the disease causes granulomatous changes in reticuloendothelial organs (granulomatous hepatitis).

When to Use Infectious

What does infectious mean? Infectious is another adjective. It means spread via the environment, and like contagious, usually refers to diseases. Infectious diseases are usually caused by bacteria, viruses, or parasites.

  • Botulism and Diphtheria are two dangerous infectious diseases.
  • Alzheimer’s disease and bipolar disorder are concerning maladies, but they are not infectious.
  • Faced with what they describe as a perfect storm of converging threats from infectious-disease epidemics, U.S. officials launched a global effort Thursday with more than two dozen countries and international organizations to prevent deadly outbreaks from spreading. –The Washington Post

The important takeaway from the word infectious is that the disease is spread through the environment, e.g., water, air, food, etc.

Many people use infectious and contagious synonymously. Even the State of Rhode Island Department of Health combines infectious and contagious diseases under the heading infectious. As careful writers, though, we must be sure not to do the same.

What is the difference between infected and infectious in epidemiology? - Biology

We compared the epidemiologic characteristics of cyclosporiasis and cryptosporidiosis in data from a cohort study of diarrhea in a periurban community near Lima, Peru. Children had an average of 0.20 episodes of cyclosporiasis/year and 0.22 episodes of cryptosporidiosis/year of follow-up. The incidence of cryptosporidiosis peaked at 0.42 for 1-year-old children and declined to 0.06 episodes/child-year for 5- to 9-year-old children. In contrast, the incidence of cyclosporiasis was fairly constant among 1- to 9-year-old children (0.21 to 0.28 episodes/child-year). Likelihood of diarrhea decreased significantly with each episode of cyclosporiasis for cryptosporidiosis, this trend was not statistically significant. Both infections were more frequent during the warm season (December to May) than the cooler season (June to November). Cryptosporidiosis was more frequent in children from houses without a latrine or toilet. Cyclosporiasis was associated with ownership of domestic animals, especially birds, guinea pigs, and rabbits.

The coccidian protozoal parasites Cyclospora cayetanensis and Cryptosporidium parvum are recognized diarrheal pathogens among children in developing countries (1–4), but longitudinal data, especially for cyclosporiasis, are sparse. Cyclospora cayetanensis is more closely related genetically to Eimeria species than to Cryptosporidium species (5), and the two organisms have biological differences. For example, C. parvum is infectious when excreted and can be transmitted directly from person to person Cyclospora cayetanensis requires a period of time in the environment to sporulate into the infectious form (3), decreasing the likelihood of direct person-to-person spread. Cryptosporidium parvum infects both humans and a variety of mammals (6), and evidence is mounting that non-parvum zoonotic Cryptosporidium species can also infect immunocompetent humans (7,8). Conversely, natural or experimental infection of animals with Cyclospora cayetanensis has not been convincingly demonstrated (9–11). Thus, cryptosporidiosis is transmitted through a variety of routes, including contaminated water or food, from person to person, or from animal to person. In contrast, the only major known risk factors for cyclosporiasis are consumption of contaminated water or produce (12–14).

Surveillance data suggest that both organisms are associated with diarrheal illness and asymptomatic infection but differ in their seasonality and susceptible age groups (15). The reasons for these differences are not well understood. Cohort studies of children in Peru provided an opportunity to better understand the characteristics of endemic cryptosporidiosis and cyclosporiasis. The objectives of the analysis were to provide a detailed description of the longitudinal epidemiology of the two organisms and to seek risk factors for infection.

Materials and Methods

Study Participants

Field work was conducted in the periurban pueblo joven (shantytown) of Pampas de San Juan de Miraflores, 25 km from the center of Lima, Peru. In the 1980s this community (pop. approximately 40,000) was heavily settled by immigrants from rural areas. Immigration to the community has slowed, and general living conditions have improved. In 1995, 97% of houses had electricity, 48% had toilets, and 64% had a household water connection (Asociación Benéfica PRISMA, Lima, Peru, unpub. data, 1995).

Our analysis was based on longitudinal data from two cohort studies conducted simultaneously from February 1995 to December 1998. The birth cohort study included all children born during the recruitment period whose mothers consented to participate its major objectives were to elucidate the relationship between diarrheal disease and nutritional status (16) and to study the epidemiology of viral gastroenteritis. The objective of the other cohort study was to examine the epidemiology of cyclosporiasis. Children from 1 month to 10 years of age were chosen at random from the complete census of the community. Siblings of birth cohort children could be enrolled in the cyclosporiasis cohort if they were chosen by random selection. Twenty sibling pairs, a number too small to allow analysis of household clustering, were included in the analysis. Excluding at random one member of each sibling pair had no effect on results, and both siblings are included in the analysis presented here.

The same epidemiologic data and specimens were collected from children in both cohort studies. At the time of recruitment, field workers collected data regarding household characteristics, including type of housing, sanitary facilities, water source, and presence of animals. Field workers visited each household daily throughout the follow-up period to compile a daily record of the presence or absence of diarrhea in the child in the primary caretaker’s opinion, number of bowel movements, and consistency of stools (liquid, semiliquid, or formed).

Stool specimens were collected weekly from all children, on the first day of a diarrheal episode, and, when one of the pathogens of interest was detected, daily until negative. Stool specimens were transported without preservative and arrived in the laboratory within 24 hours of collection. Each specimen was processed by a standard ether concentration procedure and examined microscopically for Cryptosporidium species on modified acid-fast Ziehl-Neelsen stained slides and for Cyclospora cayetanensis on wet mount by direct examination and epifluorescence (17,18) in the pathology laboratory of the Universidad Peruana Cayetano Heredia.

Epidemiologic Analysis

We defined a day with diarrhea as a 24-hour period during which the child was reported to have three or more liquid or semiliquid stools and, in addition, was thought by his or her primary caretaker to have diarrhea. An episode of diarrhea was considered to end when the child had at least 3 consecutive days that did not meet the criteria for a day with diarrhea. An episode of cryptosporidiosis or cyclosporiasis was defined by one or more stool specimens positive for the respective parasite. An episode of infection was considered to end on the last day of oocyst detection, followed by at least three negative stools and no oocyst detection for at least 28 days. An episode of infection was associated with diarrhea if at least 1 day met the definition for a day with diarrhea during the infection episode or within 1 week of the beginning or end of the episode.

We included children in the epidemiologic analysis if they had been monitored for at least 6 months and at least 24 stool specimens had been submitted for analysis. All statistics were calculated with SAS for Windows, version 8.0. We tested for seasonality and trends associated with diarrhea and infection order by Poisson regression analyses in SAS Proc Genmod (SAS, Cary, NC), incorporating generalized estimating equations to account for correlation between multiple observations from the same person. We assumed an exchangeable correlation structure. Relative risks were assessed for significance by the chi-square test. All statistical results were evaluated at the 0.05 level of significance.


Of 533 children originally recruited for the cohorts, 368 children (201 [55%] boys) met our inclusion criteria. The 165 excluded children were comparable in age and sex distribution with study children for 25 children, no stool specimen was submitted, while <6 months of surveillance was completed for the others. At the time of entry into the study, 256 children (70%) were <1 year, 45 (12%) were 1–4 years, and 67 (18%) were 5–11 years of age. The 368 children contributed a total of 889 child-years of surveillance data nearly half the data were from children <2 years of age. Children were followed for a mean of 2.4 years and had an average of 1.95 episodes of diarrhea/child-year of follow-up. The highest incidence of diarrhea, 3.3 episodes/child-year, was recorded in children 12–23 months old after the age of 3 years the incidence of diarrhea declined to <1 episode/child-year. The median duration of diarrheal episodes was 2 days (range 1–27). A total of 44,042 stool specimens were screened for coccidian parasites, a median of 124 stools/child (range 24–227) 897 (2%) of the stool specimens were collected during diarrheal episodes.

Children had an average of 0.20 episodes of cyclosporiasis/year and 0.22 episodes of cryptosporidiosis/year of follow-up (Table 1). Of the 368 children, 123 (33%) had at least one detected episode of Cyclospora infection, 30 children had two infections, and 10 children had > 3 infections. A total of 143 children (39%) had at least one Cryptosporidium infection 34 children had two infections, and 9 had > 3 infections. Rates varied by age: the incidence of cryptosporidiosis peaked at 1 year and then fell sharply, but cyclosporiasis incidence remained fairly constant during the 1- to 9-year age period. For the 189 children who were enrolled in the study before the age of 3 months, the mean age at first infection was older for cyclosporiasis than for cryptosporidiosis (1.69 versus 1.36 years p<0.01). After an initial episode of cyclosporiasis, the likelihood of diarrhea decreased significantly (p=0.049) with each subsequent infection (Table 2). For cryptosporidiosis, this trend was less consistent and did not reach statistical significance.

In a regression analysis in which data were controlled for concurrent cyclosporiasis, the expected mean duration of oocyst shedding was longer for cryptosporidiosis associated with diarrhea than for cryptosporidiosis not associated with diarrhea (expected mean 9.4 versus 4.8 days p=0.0002). In the analogous regression analysis for concurrent cryptosporidiosis, a similar relationship was found for Cyclospora cayetanensis shedding with and without diarrhea (15.7 days versus 6.2 days p=0.004). Diarrheal episodes associated with cryptosporidiosis, but not cyclosporiasis, lasted longer than diarrheal episodes not associated with coccidian parasites (expected mean duration 4.67 days for cryptosporidiosis versus 2.55 days with no coccidia p<0001 mean 2.96 days for cyclosporiasis versus 2.55 days with no coccidia p=0.35).

Both parasitic infections were more frequent during December to May than June to November, but the effect was more marked for cyclosporiasis (relative risk [RR] 3.3 p<0.0001) than for cryptosporidiosis (RR 1.9 p<0.0001). After data were adjusted for seasonality and age, the risk for cyclosporiasis or cryptosporidiosis did not differ by household water supply at the time of entry into the study (Table 3). Using a field rather than a toilet or latrine for defecation was associated with a higher risk of cryptosporidiosis but not cyclosporiasis. No association with exposure to animals could be demonstrated for cryptosporidiosis, but cyclosporiasis was more common in children in households with avians, guinea pigs, rabbits, or any other domestic animal.


Our analysis confirms that cryptosporidiosis and cyclosporiasis are common infections in this community, with distinct age-related patterns of occurrence. As noted (4,15), cyclosporiasis affected cohort children at later ages than cryptosporidiosis. The reasons for this epidemiologic pattern are not clear. One possible explanation might be that early infections afford less effective immunity for Cyclospora cayetanensis than for Cryptosporidium parvum. However, our data appear to contradict this hypothesis: first episodes of cyclosporiasis, but not cryptosporidiosis, protect against later symptomatic infection with the same organism. The development of better laboratory tools will be essential to elucidate the immune mechanisms involved. Another possibility is that the differences in age-specific incidence are related to predominant modes of exposure. This hypothesis is consistent with the assumption that Cyclospora cayetanensis is usually transmitted by exposure to contaminated environmental sources, from which young infants are usually relatively protected, while cryptosporidiosis can be transmitted by many routes, including from one toddler to another.

The ability of cryptosporidiosis to cause multiple symptomatic episodes may also be related to genetic heterogeneity. In a previous study of specimens from the same cohort, most cryptosporidiosis in this shantytown was caused by the Cryptosporidium parvum human genotype. However, children also had infections with C. parvum bovine and dog genotypes, C. meleagridis, and C. felis (8). Heterologous immunity may be less effective than homologous immunity. Although some polymorphism has been demonstrated in Cyclospora cayetanensis isolates (19), genetic studies are still in the early stages, and, to date, this parasite appears to be less heterogeneous than Cryptosporidium species. Nevertheless, immunity to both organisms occurs in this highly endemic setting, since immunocompetent adults rarely experience symptomatic infections (4).

For both coccidia, we found a high proportion of infections without diarrhea: 67% of cryptosporidiosis and 77% of cyclosporiasis episodes were not associated with diarrhea. These results differ from those reported in studies with different designs and reflect our methods, which aimed to detect as many coccidial infections as possible, independent of symptoms. Each child had a stool specimen screened nearly every week, so that 98% of the stool specimens were not collected during diarrheal episodes. Nevertheless, serologic data suggest that even intensive stool surveillance may miss a substantial proportion of cryptosporidiosis episodes (20). Data from the same Peruvian community showed that cryptosporidiosis without diarrhea had a substantial effect on childhood growth (21,22) because such infections may have long-term sequelae it is somewhat misleading to call them asymptomatic.

Cryptosporidium species infect a wide range of mammalian hosts and can be zoonotic infections (6), while Cyclospora cayetanensis has never been convincingly demonstrated to infect a nonhuman host (9–11). However, the animals most commonly associated with zoonotic C. parvum were rare in this urban setting: no families had calves, only one family had goats and lambs, and six families had adult sheep. This finding may explain why we could not show an association of cryptosporidiosis with animal exposure. Children in households with animals, especially birds, guinea pigs, and rabbits, appeared to be at higher risk of cyclosporiasis. The finding of an association with avians is consistent with results of a C. cayetanensis case-control study in Guatemala (14), but this association is still unexplained. Possibly the presence of domestic animals is a marker for some other unmeasured risk factor. Cyclosporiasis appears to be much more common in Lima than in the mountains of Peru (Asociación Benéfica PRISMA, Lima, Peru, unpub. data), and most residents of the study community migrated from the mountains to Lima. Raising domestic animals, especially poultry, may be more common among recent rural migrants with less exposure and therefore higher susceptibility to C. cayetanensis.

Our exposure data were collected at the beginning of longitudinal surveillance, and the time that elapsed between their collection and the occurrence of an infection could have been as long as several years, which may have decreased our ability to detect associations. Studies specifically designed to identify risk factors close to the time of an infection and use of molecular techniques to distinguish genotypes or strains may help clarify some of these issues.

As more longitudinal data become available for these organisms, we are gaining a clearer picture of the overall epidemiology of cyclosporiasis and cryptosporidiosis in endemic settings. Both organisms cause a spectrum of disease, from apparently asymptomatic infection to prolonged episodes of diarrhea that may have a profound effect on a child’s well-being. Our findings for cryptosporidiosis are consistent with the view that the organism infects children very early in life and has multiple routes of transmission, but mysteries remain concerning the cycle that maintains cyclosporiasis as an endemic infection. In-depth study of the transmission of C. cayetanensis will be key to designing effective strategies for intervention.

Dr. Bern is a medical epidemiologist in the Division of Parasitic Diseases, Centers for Disease Control and Prevention. Her research interests include the epidemiology of the enteric parasites Cyclospora and Cryptosporidium and microsporidia.

What is Infectious Disease Epidemiology? (with pictures)

Infectious diseases are illnesses caused by organisms that enter the body, develop, and multiply. These organisms can be bacteria, protozoans, fungi, or viruses. Epidemiology is a branch of medicine that concerns the research of the causes, distribution, and control of diseases as they relate to a particular population. Infectious disease epidemiology, therefore, generally focuses on tracing the causes of communicable diseases within a community.

Many infectious diseases are currently managed with the aid of modern medicine — new communicable diseases, such as West Nile virus and SARS, however, may present more challenges. Infectious disease epidemiology is also proving that older diseases, like tuberculosis and malaria, may now present in forms that are more resistant to established treatments. Professionals in the field of infectious disease epidemiology play a crucial role in managing the effects of both old and emerging illnesses.

An epidemiologist is a medical scientist who specializes in researching and documenting factors that influence the development of diseases. In order to work in the field, an epidemiologist must have at least a master's degree from a school of public health. Epidemiologists most often study communicable diseases and collaborate with other medical professionals to focus on prevention and control. This specialty is known as infectious disease epidemiology.

Infectious disease epidemiologists may work in research or clinical settings. A researcher in the field typically focuses on eradicating and controlling communicable diseases. He may also focus on researching particular infectious diseases, such as tuberculosis, HIV, and influenza. This type of medical professional may work at schools of public health, colleges or universities, and medicals schools.

Clinical infectious disease epidemiologists may work in hospitals to formulate guidelines for the management of various communicable diseases. They may also serve as consultants to hospital medical staff in the control of infectious diseases. These epidemiologists collect and analyze laboratory results, geographic distribution, and severity of such conditions.

Some universities offer certificate programs for those who wish to gain graduate-level training in infectious disease epidemiology. These are typically structured as non-degree programs. Individuals who may benefit from this type of certification include laboratory professionals, nurses, veterinarians, and various physicians.

Many government health departments maintain their own infectious disease epidemiology programs. These initiatives help to monitor and control infectious diseases, including those that can be prevented by vaccines, such as bacterial meningitis. These programs also track food and waterborne illnesses, such as E. coli vectorborne conditions, like West Nile virus and zoonotic diseases, such as the plague. Such governmental groups are typically responsible for investigating outbreaks of these illnesses within their jurisdiction. The programs may also serve as information resources to healthcare providers, offering medical consultations in various cases.

Help stop the spread of COVID-19 and other infectious diseases in developing countries

The COVID-19 pandemic has meant that infectious disease is in the headlines throughout the world. COVID-19, however, is not the only infectious disease affecting developing communities in countries across South East Asia.

You can help stop the spread of infectious diseases. When you donate to our current appeal, your donation provides improved access to healthcare facilities, funds outreach clinics, trains healthcare workers and more. Please donate.


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