Infectivity and oocyst excretion patterns of Cryptosporidium muris in slightly infected mice

To determine the infectivity of Cryptosporidium to hosts in slight infections, we examined the infectivity and oocyst output patterns of Cryptosporidium muris in mice inoculated with small numbers of oocysts. One of the 25 ICR mice inoculated with 2.4 x 10(1) oocysts and 19 of the 25 mice inoculated with 2.4 x 10(2) oocysts shed oocysts in the feces after inoculation. Four of the 50 mice inoculated with 2.4 x 10(1) oocysts for 10 consecutive days also shed oocysts and their OPG values were similar to that of the mice which received 2.4 x 10(2) oocysts. Consequently, it is clear that less than 10% of the mice which received 2.4 x 10(1) C. muris oocysts for 10 consecutive days.     

Infectivity to experimental rodents of Cryptosporidium parvum oocysts from Siberian chipmunks (Tamias sibiricus) originated in the People's Republic of China

We isolated Cryptosporidium parvum-type oocysts from naturally infected siberian chipmunks which originated in the People's Republic of China and examined the infectivity to rodents as experimental animals. The naturally infected chipmunks did not show any clinical symptoms. The oocysts were 4.8 x 4.2 microm on average in size. They were ovoid and morphologically similar to the C. parvum oocysts isolated from human and cattle. Experimental rodents were inoculated with 1.6 x 10(6) original oocysts each. SCID mice began to shed oocysts on day 7 and the OPG value was 10(5) from 50 days. The oocysts were found from ICR mice on days 13 and 16 by only sugar flotation method, however, any oocysts were not detected from the rats, guinea pigs and rabbits until 30 days. Two infected SCID mice were necropsied on days 100 and 102 and examined for coccidian organisms. Merozoites and oocysts were found in the low part of jejunum and ileum, however, no parasites were detected in the stomach. Consequently, it was considered that the present species was C. parvum and was probably genotype 2 from result of infectivity to rodents.     

Infectivity of Cryptosporidium parvum isolated from asymptomatic adult goats to mice and goat kids.

An experimental study was carried out in neonatal goat kids to examine the infectivity of Cryptosporidium oocysts, pattern of oocyst shedding and morphological changes in the intestine during the infection. Cryptosporidium oocysts isolated from adult asymptomatic goats, and identified as C. parvum by polymerase chain reaction (PCR) were used in this study. Of three 4-day-old goat kids, two were orally infected with C. parvum oocysts (10(5) oocysts in 10 ml PBS/kid). One goat kid given 10 ml PBS only by the oral route served as a control. Cryptosporidium oocysts were detected in the faeces of one infected kid on day 3 post-inoculation (pi) whereas in the other 6 days pi. The faecal oocyst counts gradually increased and the peak counts in the two kids were 2 x 10(6)g(-1) (on day 12 pi) and 3.2 x 10(6)g(-1) (on day 14 pi). The increase in faecal oocyst output coincided with diarrhoea in an infected kid from days 10-17 pi. Although the oocyst excretion declined gradually after the peak, both infected kids excreted oocysts until euthanized on days 20 and 22 pi. Light and scanning electron microscopic investigations of the ileum revealed the endogenous stages on the brush border of the enterocytes, infiltration of neutrophils and mononuclear cells into the lamina propria, atrophy, stunting and fusion of villi. For purposes of comparison, goat Cryptosporidium oocysts were inoculated orally (10(3) oocysts/mouse) to eight, 1-week-old mice. All experimental mice excreted oocysts from day 3 pi, and four infected mice continued to excrete oocysts up to day 42 pi. The experimental infection described in goat kids resembled the natural disease in terms of oocyst excretion, clinical signs and intestinal pathology. The ability of oocysts excreted by asymptomatic goats, to infect goat kids and mice is likely to have a major impact on the epidemiology of cryptosporidiosis in livestock and man.     

Infectivity of a novel type of Cryptosporidium andersoni to laboratory mice

Previously, we reported 'a novel type' of Cryptosporidium andersoni detected from cattle in Japan, and showed that the isolate was infective to mice. In the present study, we examined the patterns of oocyst shedding in both immunocompromised and immunocompetent mice, as well as pathological lesions in the infected mice. After oral inoculation with 1 x 10(6) oocysts, all five severe combined immunodeficiency (SCID) mice began to shed endogenously produced oocysts on day 6 post-inoculation (p.i.). The number of oocysts per day (OPD) reached 1 x 10(6) on day 17 p.i., and an OPD level of 1 x 10(6) to 10(7) was maintained until 91 days p.i. when the mice were sacrificed. In the five immunocompetent mice inoculated with 1 x 10(6) oocysts, the pre-patent and patent periods were 6 and 19 days, respectively, and the maximal OPD level was 1.5 x 10(5) on average. On histological examinations of infected SCID mice, a large number of parasites were present on the surface of the gastric glands of the stomach, but not in other organs examined. In conclusion, the novel type of C. andersoni, which genetically coincides with C. andersoni reported in other countries, is infective to mice, but susceptibility was lower than that of Cryptosporidium muris infecting rodents from the perspective of infectivity to immunocompetent mice.     

Infectivity of Cryptosporidium sp isolated from wild mice for calves and mice

A study was conducted to determine the incidence of cryptosporidiosis in wild mice (Mus musculus) and the infectivity of oocysts from their feces for susceptible calves. The presence of oocysts and the duration of shedding of oocysts in the feces were evaluated in 115 wild mice. Approximately 30% of the mice shed Cryptosporidium sp oocysts, without evidence of clinical infection; recurrence of oocyst shedding was found in about 50% of the mice. Oocysts from the feces of naturally infected mice were infective for calves and mice. Calves began shedding oocysts at 7 days and shed oocysts for about 10 days. Nonfatal, clinical cryptosporidiosis developed in 7 infected calves. The mice began shedding oocysts at 6 days and shed oocysts for 12 days. Fatalities or clinical infection did not develop in 5 infected mice. The results indicated that Cryptosporidium-infected wild mice may be a source of cryptosporidiosis in susceptible calves.     

Life cycle of Eimeria krijgsmanni-like coccidium in the mouse (Mus musculus)

Life cycle of Eimeria krijgsmanni-like coccidium isolated from the feces of naturally infected mice purchased from commercial sources was examined. The parasite was purified by single oocyst isolation and maintained by passage in the mice before experiments. The sporulated oocysts were ovoid or ellipsoid, measuring 19.3 x 14.8 microm on average. One or two small polar granules were present. Micropyle and oocyst residuum were absent. Sporocysts were ellipsoid, measuring 11.6 x 7.2 microm on average with a small Stieda body and sporocyst residuum. Six groups of respective 5 mice (4-week-old) were inoculated with doses varying from 2.0 x 10(1) to 10(6) oocysts. All the mice examined began to shed oocysts from 7 day postinoculation (PI) and their maximum number of oocysts per gram of feces were 10(6) on day 8 PI. Patency was 6 or 7 days. This parasite had severe virulence to the mice that is, the mice given 10(6) oocysts showed anorexia, diarrhoea and rough hair from 1 day and all of them died on day 3 PI. The mice given 10(3) or more oocysts showed the clinical signs described above from day 5 and 4 of them received 10(5) died on day 9 or 10 PI. The parasites occurred within the epithelial cells of cecum, colon and rectum of infected mice. Sporozoites, 13.9 x 3.0 microm, with two large refractil bodies on side of the nucleus located subcentrally were observed on day 1 and 2 PI. Merozoites were first observed at 24 hr PI, and sexual stages were found from 4 day PI. No parasites were detected in the small intestine and mecenteric lymph nodes.     

Effects of low and high temperatures on infectivity of Cryptosporidium muris oocysts suspended in water

Cryptosporidium muris oocysts suspended in 200 microl of water were pipetted into plastic microcentrifuge tubes which were stored at 4 degrees C or frozen at -5 degrees C for 1, 3, 5, 7, and 10 days and at -20 degrees C for 1, 3, 5, and 8h, respectively. Other samples of C. muris oocysts suspended in water were heated in the metal block of a thermal DNA cycler. Block temperatures were set at 5 degrees C incremental temperatures from 40 to 70 degrees C. At each high temperature setting microcentrifuge tubes containing C. muris oocysts were exposed for 1 min. Both, frozen and heated oocyst suspensions as well as untreated control oocyst suspensions were then inoculated into each of four ICR mice by gastric intubation. Untreated, freeze-thawed or heated oocysts were considered infectious when oocysts of C. muris were found microscopically in the faeces of mice after inoculation. All inoculated mice that received oocysts frozen at -5 degrees C for 3, 5, 7, and 10 days and -20 degrees C for 1, 3, 5, and 8h had no oocysts in faeces. In contrast, C. muris oocysts frozen at -5 degrees C for 1 day remained infective for inoculated mice. Our results also indicated that when water containing C. muris oocysts was exposed at a temperature of 55 degrees C or higher for 1 min, the infectivity of oocysts was lost.     

Experimental infection of budgerigars (Melopsittacus undulatus) with a low virulent K21 strain of Toxoplasma gondii

In total 53 budgerigars (Melopsittacus undulatus) were divided into six groups and orally infected with a suspension of oocysts of low virulent Toxoplasma gondii K21 strain in the doses of 10(2), 10(3), 10(4), 10(5) and 10(6), respectively. Blood was collected from the birds prior to the inoculation and then on days 10, 20 and 30 post infection. Latex-agglutination test (LAT) was used for the detection of antibodies in the inoculated birds. The infected birds showed no apparent signs of disease. The antibodies were found in all but two birds inoculated a dose of 10(2) oocysts. Haematological values remained unchanged after infection. T. gondii was isolated by bioassay in mice from all 37 birds fed 10(3) or more oocysts and 6 of 9 fed 10(2) oocysts. The results demonstrate that budgerigars are resistant to T. gondii infection.     

Protective immunity to toxoplasmosis in pigs vaccinated with a nonpersistent strain of Toxoplasma gondii

The RH strain of Toxoplasma gondii is highly virulent; 1 infective organism is uniformly lethal for mice. Three pigs inoculated SC with 10(3) tachyzoites of the RH strain developed fever, but otherwise remained normal, and T gondii was not demonstrated in their tissues by bioassay into mice. To determine whether vaccination with the RH strain could induce protective immunity to oral challenge with T gondii oocysts, 12 pigs were divided into 3 groups (A, B, C) of 4 pigs each. Pigs in groups A and B were inoculated IM with 10(6) tachyzoites of the RH strain and 4 pigs in group C served as uninoculated controls. Except for fever, the pigs remained clinically normal after inoculation with the RH strain and T gondii was not found by bioassay in mice of tissues from 4 pigs euthanatized 64 days after inoculation. Pigs in groups B and C were challenge-inoculated orally with 10(4) (4 pigs) or 10(5) (4 pigs) T gondii oocysts 72 days after vaccination with the RH strain. The previously uninoculated pigs developed fever, anorexia, and diarrhea from 3 to 8 days after the oocyst challenge. One of the 2 pigs given 10(5) oocysts became moribund because of toxoplasmosis and was euthanatized 9 days after inoculation. Pigs vaccinated with the RH strain remained free of clinical signs after challenge with oocysts. Results of the bioassays indicated that fewer tissue cysts developed in the RH strain-vaccinated pigs than in the previously uninoculated control pigs.     

Malabsorption of vitamin A in preruminating calves infected with Cryptosporidium parvum.

Serum retinol, retinyl palmitate, and total vitamin A concentrations, and jejunoileal morphology were examined in neonatal calves infected with Cryptosporidium parvum. Group-1 calves served as noninfected controls and, after an adjustment period, were given 50 ml of saline solution i.v. every 12 hours for 6 days. Group-2 calves were inoculated with 10(7) C parvum oocysts and, after the onset of diarrhea, were given 50 ml of saline solution i.v. every 12 hours for 6 days. Group-3 calves were inoculated with 10(7) C parvum oocysts and, after the onset of diarrhea, were treated with difluoromethylornithine (DFMO, 200 mg/kg of body weight i.v., q 12 h) for 6 days. Group-4 calves were naturally infected with C parvum. Jejunoileal biopsy specimens were excised from calves of groups 1-3 at 3 and again at 15 to 16 days of age. During the course of diarrhea and 3 days after saline or DFMO administration, water-miscible retinyl palmitate was administered orally (2,750 micrograms/kg) to each calf in each group. Cryptosporidium parvum infection was associated with significant (P < or = 0.05) reduction in postadministration serum retinol, retinyl palmitate, and total vitamin A concentrations in calves of groups 2, 3, and 4. Cryptosporidium parvum infection caused significant (P < or = 0.05) reduction in villus height. Decreased villus height, villus blunting and fusion, and attenuation of the intestinal mucosa were associated with reduced absorption of vitamin A, as indicated by lower peak postadministration retinyl palmitate concentration in C parvum-infected calves. Intravenous administration of DFMO to group-3 calves did not improve retinol absorption.(ABSTRACT TRUNCATED AT 250 WORDS)     

Experimental cryptosporidiosis and infectious bursal disease virus infection of specific-pathogen-free chickens

Specific-pathogen-free chickens orally inoculated at 4 days of age with a moderately pathogenic vaccine strain of infectious bursal disease virus (IBDV) and/or at 5 days of age with Cryptosporidium baileyi oocysts remained free of overt clinical signs throughout a 16-day period postinoculation (PI). The prepatency period for C. baileyi oocyst shedding was shorter in chickens receiving higher numbers of oocysts, but once shedding was detected, there were no obvious differences in shedding patterns among groups receiving 10(3) through 10(6) oocysts. On days 8 and 16 PI, cryptosporidia were located primarily in the bursae of Fabricius. IBDV exposure was associated with bursal follicle atrophy, whereas C. baileyi infection resulted in bursal epithelial hypertrophy and hyperplasia, mild follicle atrophy, and heterophil infiltration of the bursal mucosa. Examination of experimental groups of 30 birds each indicated that concurrent infection with both agents resulted in more severe bursal lesions, more infected birds, and greater numbers of cryptosporidia in infected tissues. At the termination of the trial, 16 days PI, Cryptosporidium infection was associated with a 6% decrease in mean body weight compared with controls.     

Effect of broiler chicken age on susceptibility to experimentally induced Cryptosporidium baileyi infection

Clinical signs of respiratory tract disease were observed in chickens that were inoculated intratracheally with 1 x 10(6) oocysts of Cryptosporidium baileyi at 2 or 14 days of age (10 chickens/group), but not in chickens inoculated at 28 or 42 days of age (10 chickens/group). Orally inoculated chickens in all age groups (10 chickens/group) did not develop clinical signs of disease. Orally and intratracheally inoculated chickens in all age groups were infected, as determined by the finding of cryptosporidia in tissue sections of the trachea, bursa of Fabricius, and cloaca, and by the recovery of oocysts from their feces. Chickens inoculated at 2 and 14 days of age excreted oocysts for a longer period and had greater numbers of cryptosporidia in their tissues, compared with chickens inoculated at 28 and 42 days of age.     

Immunity to Hammondia hammondi infection in cats.

Acquisition of immunity to Hammondia hammondi, a newly recognized coccidian of cats, was studied in 18 specific-pathogen-free cats. One cat was given a single oral inoculation, 11 cats were given 2 oral inoculations, and 1 cat was given 3 oral inoculations of homogenized mouse carcasses containing H hammondi. In all cats, oocyst shedding began 6 to 9 days after the 1st inoculation. Oocyst shedding peaked at 1 to 2 days after the onset of shedding and lasted for 1 to 2 weeks. None of the cats became sick. Of the 11 cats inoculated twice (between 2-51 days after the 1st inoculation), 5 shed oocysts 7 to 14 days after the repeat inoculation; however, fewer oocysts were shed at this time. One cat that was inoculated thrice (14 and 51 days after the 1st inoculation) shed oocysts 14 to 17 days after the 3rd inoculation but not after the 2nd inoculation. Spontaneous oocyst shedding was studied in 9 of these 13 H hammondi-infected cats for 5 months. Two cats spontaneously shed oocysts: One cat (inoculated only once) spontaneously re-shed oocysts 21 to 24, 31 to 33, 49 to 50, and 118 to 120 days after inoculation; The other cat (inoculated twice-the 2nd time, 6 days after the 1st inoculation) re-shed oocysts 38 to 48, 85 to 89, and 133 to 136 days after the 1st inoculation. The course of H hammondi infection was studied in 5 cats given weekly injections of 6-methyl prednisolone acetate for at least 7 weeks, starting 18 days before inoculation in 2 cats, and starting 14, 34, and 45 day after inoculation in 3 cats. The induced hyperadrenocorticism did not affect the prepatent period or induce parasitism of extraintestinal organs. The 3 cats infected for 14, 34, and 45 days, re-shed oocysts after hyperadrenocorticism was induced. It was concluded that immunity to H hammondi infection in cats is less stable than immunity to the related coccidian, Toxoplasma gondii.     

Viability and infectivity of Cryptosporidium parvum oocysts detected in river water in Hokkaido,Japan

The viability and infectivity of Cryptosporidium parvum (C. parvum) oocysts, detected in water samples collected from river water in Hokkaido, were investigated using Severe Combined Immunodeficient (SCID) mice. The water samples collected from September 27 through October 10, 2001 by filtration using Cuno cartridge filters were purified and concentrated by the discontinuous centrifugal flotation method. From 1.2 x 10 (5) liters of the raw river water, approximately 2 x 10(4) oocysts were obtained and designated as Hokkaido river water 1 isolate (HRW-1). Oocyst identification was carried out using microscopic and immunological methods. Six 8-week-old female SCID mice were each inoculated orally with 1 x 10 (3) oocysts. Infection was successfully induced, resulting in fecal oocyst shedding. Oocysts were then maintained by sub-inoculation into SCID mice every 3 months. Infectivity was evaluated by making comparisons with two known C. parvum stocks, HNJ-1 and TK-1, which were bovine genotypes detected in fecal samples from a cryptosporidiosis patient and young cattle raised in Tokachi, Hokkaido respectively. The oocyst genotypes were determined from a small subunit ribosomal RNA (SSU-rRNA) gene by polymerase chain reaction - restriction fragment length polymorphism (PCR-RFLP) analysis. No significant differences were observed in the average number of oocysts per gram of feces (OPG) in any of the isolates. Our data indicates that the C. parvum oocysts detected in the sampled river water were of C. parvum genotype 2. Moreover, our data on the continued isolation, detection and identification of the C. parvum isolates is consistent with the available epidemiological data for the Tokachi area.     

Unexpected oocyst shedding by cats fed Toxoplasma gondii tachyzoites: in vivo stage conversion and strain variation

Tachyzoites, bradyzoites (in tissue cysts), and sporozoites (in oocysts) are the three infectious stages of Toxoplasma gondii. The prepatent period (time to shedding of oocysts after primary infection) varies with the stage of T. gondii ingested by the cat. The prepatent period (pp) after ingesting bradyzoites is short (3-10 days) while it is long (18 days or longer) after ingesting oocysts or tachyzoites, irrespective of the dose. The conversion of bradyzoites to tachyzoites and tachyzoites to bradyzoites is biologically important in the life cycle of T. gondii. In the present paper, the pp was used to study in vivo conversion of tachyzoites to bradyzoites using two isolates, VEG and TgCkAr23. T. gondii organisms were obtained from the peritoneal exudates (pex) of mice inoculated intraperitoneally (i.p.) with these isolates and administered to cats orally by pouring in the mouth or by a stomach tube. In total, 94 of 151 cats shed oocysts after ingesting pex. The pp after ingesting pex was short (5-10 days) in 50 cats, intermediate (11-17) in 30 cats, and long (18 or higher) in 14 cats. The strain of T. gondii (VEG, TgCKAr23) or the stage (bradyzoite, tachyzoite, and sporozoite) used to initiate infection in mice did not affect the results. In addition, six of eight cats fed mice infected 1-4 days earlier shed oocysts with a short pp; the mice had been inoculated i.p. with bradyzoites of the VEG strain and their whole carcasses were fed to cats 1, 2, 3, or 4 days post-infection. Results indicate that bradyzoites may be formed in the peritoneal cavities of mice inoculated intraperitoneally with T. gondii and some bradyzoites might give rise directly to bradyzoites without converting to tachyzoites.     

Control of bovine coccidiosis with monensin: in nonresistant newborn calves

Newborn Holstein male calves were purchased within 3 days after birth and were removed from the local farms to the Dixon Springs Agricultural Research Center. They were hand-fed for 7 weeks and then weaned to a prepared feed. Eight groups, each of 4 calves, were housed in separate pens. In each of 4 pens (pens 2 to 5), 1 calf was inoculated with sporulated oocysts of Eimeria bovis (and was not medicated); 1 calf was inoculated and given feed with added monensin at the dosage level of 10 g/906 kg of feed; and 2 calves were inoculated and given medicated feed with added monensin at the dosage level of 20 g/906 kg or 30 g/906 kg. In the 4 other pens (6 to 9), the calves were inoculated with E zuernii and otherwise were given feed without or with added monensin as in pens 2 through 5. Another group of 5 calves (all kept in 1 pen), served as noninoculated, nonmedicated controls. At 14 days after inoculations with E bovis, the single calves in each of the 4 pens that were given the nonmedicated feed began to show clinical signs of coccidiosis and discharged increasing numbers of oocysts. The other inoculated calves (given monensin) had fewer clinical signs and discharged fewer oocysts in the feces as the level of medication in the feed increased. The calves inoculated with E zuernii developed only moderately severe infections when compared with those inoculated with E bovis. Inoculated (with E bovis) nonmedicated calves had severe reductions in feed consumption and weight, and 3 of 4 died.(ABSTRACT TRUNCATED AT 250 WORDS)     

Number of Cryptosporidium parvum oocysts or Giardia spp cysts shed by dairy calves after natural infection

OBJECTIVE: To determine the total number of Cryptosporidium parvum oocysts and Giardia spp cysts shed by dairy calves during the period when they are most at risk after natural infection. ANIMALS: 478 calves naturally infected with C. parvum and 1,016 calves naturally infected with Giardia spp. PROCEDURE: Oocysts or cysts were enumerated from fecal specimens. Distribution of number of oocysts or cysts versus age was used to determine the best fitting mathematic function. Number of oocysts or cysts per gram of feces for a given duration of shedding was computed by determining the area under the curve. Total number of oocysts or cysts was calculated by taking the product of the resultant and the expected mass of feces. Results: Intensity of Cparvum oocyst shedding was best described by a second-order polynomial function. Shedding increased from 4 days of age, peaked at day 12, and then decreased. An infected 6-day-old calf would produce 3.89 x 10(10) oocysts until 12 days old. Pattern of shedding of Giardia spp cysts was best described by exponential functions. Intensity of shedding increased from 4 days of age, peaked at day 14, and then decreased. An infected calf would produce 3.8 x 10(7) cysts from day 50 until day 56. CONCLUSIONS AND CLINICAL RELEVANCE: The large number of oocysts and cysts shed indicates that shedding by dairy cattle poses a risk for susceptible calves and people. Estimates reported here may be useful to aid in designing cost-effective strategies to manage this risk.     

Evaluation of lasalocid as a coccidiostat in calves: titration, efficacy, and comparison with monensin and decoquinate

Two experiments were conducted to evaluate lasalocid as a coccidiostat in Holstein calves and to compare lasalocid with monensin and decoquinate. In experiment 1, calves in 3 groups (6 calves/group) were each inoculated with 500,000 sporulated oocysts, 88% of which were Eimeria bovis and 12% were E zuernii. Calves in each group were given lasalocid-medicated feed at 0.50 (group 3), 0.75 (group 4), or 1 mg/kg (group 5) of body weight/day for 45 days. Two control groups (6 calves/group) were also evaluated; calves in control group 2 were inoculated and nontreated, and calves in control group 1 were noninoculated and nontreated. At 0.50, 0.75, or 1 mg/kg/day, lasalocid was equally effective in preventing induced coccidiosis (E bovis and E zuernii) in calves. Compared with inoculated nontreated controls, treated calves had significantly (P less than 0.05) fewer oocysts in feces and had fewer clinical signs of coccidiosis from days 16 to 30 after inoculation. Experiment 2 was conducted to compare the effectiveness of monensin, lasalocid, and decoquinate for the prevention of experimentally induced coccidiosis. Calves (n = 48) were allotted into 4 groups (12 calves/group); each was inoculated orally with 275,000 sporulated oocysts, predominantly E bovis and E zuernii, and each was given nonmedicated feed (group 6) or feed medicated with 33 mg of lasalocid (group 7), decoquinate (group 8), or monensin (group 9)/kg of feed for 46 days. Calves given medicated rations had significantly (P less than 0.05) fewer oocysts in their feces and fewer clinical signs of coccidiosis than did calves given nonmedicated rations.(ABSTRACT TRUNCATED AT 250 WORDS)     

Fecal shedding of Cryptosporidium oocysts in healthy alpaca crias and their dams

Objective-To determine the apparent prevalence of shedding of Cryptosporidium spp in healthy alpaca crias and their dams on 14 farms in New York and 1 farm in Pennsylvania. Design-Cross-sectional study. Animals-110 alpaca crias and their 110 dams. Procedures-Fecal samples were obtained from 220 alpacas at 14 alpaca farms in New York and 1 farm in Pennsylvania. For each animal, age, sex, and health condition were recorded. A fecal score (1 = normally formed; 2 = soft or loose; 3 = diarrhetic) was recorded for each cria. Cryptosporidium oocysts were identified in fecal samples by a direct immunofluorescence assay. Results-Apparent prevalence of fecal shedding of Cryptosporidium oocysts was 8% (95% confidence interval, 4% to 15%) in dams and was 7% (95% confidence interval, 3% to 13%) in crias. There was no significant difference in age between dams with positive fecal test results for Cryptosporidium oocysts (median age, 4 years; range, 3 to 8 years) and dams with negative results (median age, 4 years; range, 2.5 to 19 years). No significant difference was found in age between crias with positive fecal test results (median age, 20 days; range, 7 to 53 days) and those with negative results (median, 36 days; range, 2 to 111 days). No significant difference in fecal scores was found between crias with positive versus negative fecal test results. Conclusions and Clinical Relevance-A higher than previously reported apparent prevalence of fecal shedding of Cryptosporidium oocysts in healthy alpacas was found. A zoonotic risk should be considered, especially for Cryptosporidium parvum.     

Duration of naturally acquired giardiosis and cryptosporidiosis in dairy calves and their association with diarrhea

OBJECTIVE: To determine duration of infection and association of infection with diarrhea for dairy calves with naturally acquired cryptosporidiosis and giardiosis. DESIGN: Cohort study. ANIMALS: 20 Holstein calves on a single dairy farm. PROCEDURE: Fecal samples were collected 3 times/wk for the first 45 days after birth, then weekly until calves were 120 days old and examined for Giardia duodenalis cysts and Cryptosporidium parvum oocysts. Calves were monitored for diarrhea during the first 45 days after birth; during each episode of diarrhea, fecal samples were examined for parasitic, bacterial, and viral pathogens. RESULTS: All 20 calves shed Giardia cysts and Cryptosporidium oocysts at some time during the study. Mean ages at which Giardia cysts and Cryptosporidium oocysts were first detected were 31.5 and 16.3 days, respectively. Mean number of Giardia cysts in feces remained high throughout the study, whereas Cryptosporidium occysts decreased to low or undetectable numbers 2 weeks after infection. Eighteen calves had a total of 38 episodes of diarrhea during the first 45 days after birth. Giardia duodenalis was the only pathogen identified during 6 (16%) episodes, C parvum was the only pathogen identified during 9 (24%) episodes, and G duodenalis and C parvum were identified together during 10 (26%) episodes. CONCLUSIONS: Prevalences of giardiosis and cryptosporidiosis were high in these calves, and both parasites were associated with development of diarrhea. Cryptosporidium parvum was an important pathogen when calves were < 1 month old, but G duodenalis was more important when calves were older. Calves cleared C parvum infections within 2 weeks; however, G duodenalis infections became chronic in these calves.